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Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder
Open accessAbstract
Major depressive disorder (MDD) is a common mental disorder associated with a significant negative impact on quality of life, morbidity/mortality, and cognitive function. Individuals who suffer with MDD display lower serum/plasmatic total antioxidant potentials and reduced brain GSH levels. Also, F2-isoprostanes circulatory levels are increased in MDD subjects and are correlated with the severity of depressive symptoms. Urinary excretion of 8-OHdG seems to be higher in patients with MDD compared to healthy controls. Despite the fact that antidepressant drugs have been used for more than 50 years, their mechanism of action is still not fully understood. This paper examines preclinical (in vitro and animal model) and clinical literature on oxidative/antioxidant effects associated with antidepressant agents and discusses their potential antioxidant-related effects in the treatment of MDD. Substantial data support that MDD seems to be accompanied by elevated levels of oxidative stress and that antidepressant treatments may reduce oxidative stress. These studies suggest that augmentation of antioxidant defences may be one of the mechanisms underlying the neuroprotective effects of antidepressants in the treatment of MDD.
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TL;DR
This review synthesizes preclinical and clinical evidence that major depressive disorder (MDD) is accompanied by elevated oxidative stress and that antidepressant treatment, especially longer-term, may reduce oxidative stress and augment antioxidant defences. It suggests that augmentation of antioxidant defences may be one mechanism underlying the neuroprotective effects of antidepressants in MDD.
Key findings
- MDD has been associated with lower serum/plasmatic total antioxidant potentials, reduced brain GSH levels, lower plasma coenzyme Q10, increased serum xanthine oxidase, increased F2-isoprostanes correlated with depressive symptom severity, and higher urinary 8-OHdG versus healthy controls.
- In vitro and animal studies mostly support antioxidant-related effects of antidepressants, but some show prooxidant effects at high doses, particularly fluoxetine in rat liver; for example, chronic fluoxetine increased liver TBARS, carbonyl groups, and uric acid, with effects more pronounced at 24 versus 8 mg/kg.
- Clinical studies suggest treatment duration matters: short-term treatments (4 to 8 weeks) do not seem to alter antioxidant/oxidative parameters, whereas longer treatments (12 to 24 weeks) seem to induce robust antioxidant effects.
- Specific clinical findings include restoration of plasmatic GPx and MDA after 12 weeks of SSRIs in 32 MDD patients; in 57 MDD patients, TOS and OSI were higher and TAC lower, with severity correlations of r = 0.58, r = 0.63, and r = −0.553, and after 3 months of treatment TOS/OSI decreased and TAC increased.
Methods
- Narrative review of preclinical (in vitro and animal model), post-mortem, and clinical literature on oxidative/antioxidant effects associated with antidepressant agents in MDD.
- Data include studies summarized in tables, with human cohorts ranging from small samples to 96 MDD patients and treatment durations from 4 to 24 weeks.
- Main analysis is qualitative synthesis of reported oxidative stress markers, antioxidant enzymes, and treatment effects; no systematic search strategy or meta-analysis is described.
Limitations
- The paper states that post-mortem studies are not conclusive mostly because of small sample sizes, lack of control groups, and lack of relevant information such as treatment duration and specific drugs used.
- The paper states that many clinical studies were short in duration and likely underpowered to address differences in antioxidant potential among particular drugs, and that larger studies are warranted.
- The paper notes that peripheral markers may not necessarily correlate with central nervous system changes, citing Teyssier et al. (2011), who found oxidative stress-response genes were not altered in the prefrontal cortex of individuals with MDD, although all patients had received antidepressant treatment. Evident from the text: the review is narrative and heterogeneous across drugs, doses, tissues, and outcome markers, limiting direct comparability.
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Claims the paper makes
102 Not checked yet · 25 Own interpretation · 1 Own method
In the paper
“increased serum XO levels observed in MDD subjects suggest increased systemic ROS production [29].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 3. Oxidative Stress in Major Depressive Disorder
What the sources say
- Not checked yetcites [29] Herken H Gurel A Selek S Adenosine deaminase, nitric oxide, superoxide dismutase, and xanthine oxidase in patients with major depression: impact of antidepressant treatment Archives of Medical Research 2007 38 2 247 252 17227736 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“A recent post-mortem study found increased XO activity in the thalamus and putamen patients with recurrent MDD [35].”
- Also stated in: § 4.3. Post-Mortem Studies · plain
“Michel et al. (2010) showed increased XO activity in the thalamus and putamen of seven individuals with an ante-mortem diagnosis of recurrent MDD (age range = 61–93 y.o.).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 3. Oxidative Stress in Major Depressive Disorder
What the sources say
- Not checked yetcites [35] Michel TM Camara S Tatschner T Increased xanthine oxidase in the thalamus and putamen in depression World Journal of Biological Psychiatry 2010 11 2 314 320 20218795 source
plaincorrelationaln = 7- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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- Also stated in: § 4.3. Post-Mortem Studies · plain
In the paper
“Plasmatic coenzyme Q10 (CoQ10), a strong antioxidant and a key molecule in the mitochondrial electron transport chain, is significantly lower in major depressive patients [34]”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 3. Oxidative Stress in Major Depressive Disorder
What the sources say
- Not checked yetcites [34] Maes M Mihaylova I Kubera M Uytterhoeven M Vrydags N Bosmans E Lower plasma Coenzyme Q10 in depression: a marker for treatment resistance and chronic fatigue in depression and a risk factor to cardiovascular disorder in that illness Neuroendocrinology Letters 2009 30 4 462 469 20010493
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“urinary excretion of 8-OHdG, a marker of oxidative damage to DNA, was found to be higher in patients with MDD than healthy controls [52].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 3. Oxidative Stress in Major Depressive Disorder
What the sources say
- Not checked yetcites [52] Maes M Mihaylova I Kubera M Uytterhoeven M Vrydags N Bosmans E Increased 8-hydroxy-deoxyguanosine, a marker of oxidative damage to DNA, in major depression and myalgic encephalomyelitis/chronic fatigue syndrome Neuroendocrinology Letters 2009 30 6 715 722 20035260
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Individuals who suffer with MDD display lower serum/plasmatic total antioxidant potentials [28, 32, 48] and reduced brain GSH levels [31] as compared to matched controls.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 3. Oxidative Stress in Major Depressive Disorder
What the sources say
- Not checked yetcites [28] Sarandol A Sarandol E Eker SS Erdinc S Vatansever E Kirli S Major depressive disorder is accompanied with oxidative stress: short-term antidepressant treatment does not alter oxidative—antioxidative systems Human Psychopharmacology 2007 22 2 67 73 17299810 source
- Not checked yetcites [32] Cumurcu BE Ozyurt H Etikan I Demir S Karlidag R Total antioxidant capacity and total oxidant status in patients with major depression: impact of antidepressant treatment Psychiatry and Clinical Neurosciences 2009 63 5 639 645 19674383 source
- Not checked yetcites [48] Gałecki P Szemraj J Bieńkiewicz M Florkowski A Gałecka E Lipid peroxidation and antioxidant protection in patients during acute depressive episodes and in remission after fluoxetine treatment Pharmacological Reports 2009 61 3 436 447 19605942 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Substantial data support that MDD seems to be accompanied by elevated levels of oxidative stress and that antidepressant treatments may reduce oxidative stress.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Findings from animal models and in vitro studies about antidepressant antioxidant effects are relevant to human MDD treatment.
- Rests on an assumption: Peripheral markers of oxidative stress (serum/plasmatic) reflect central/brain oxidative stress in MDD.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Substantial data support that MDD seems to be accompanied by elevated levels of oxidative stress and that antidepressant treatments may reduce oxidative stress.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > Abstract
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Findings from animal models and in vitro studies about antidepressant antioxidant effects are relevant to human MDD treatment.
- Rests on an assumption: Peripheral markers of oxidative stress (serum/plasmatic) reflect central/brain oxidative stress in MDD.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These studies suggest that augmentation of antioxidant defences may be one of the mechanisms underlying the neuroprotective effects of antidepressants in the treatment of MDD.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Findings from animal models and in vitro studies about antidepressant antioxidant effects are relevant to human MDD treatment.
- Rests on an assumption: Peripheral markers of oxidative stress (serum/plasmatic) reflect central/brain oxidative stress in MDD.
In the paper
“Kolla et al. (2005) have demonstrated that pretreatment with amitriptyline and fluoxetine protects against oxidative stress-induced damage in rat pheochromocytoma (PC12) cells.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [10] Kolla N Wei Z Richardson JS Li XM Amitriptyline and fluoxetine protect PC12 cells from cell death induced by hydrogen peroxide Journal of Psychiatry and Neuroscience 2005 30 3 196 201 15944744 PMC1089780
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“Both drugs attenuated the decrease in cell viability induced by H2O2 in PC12 cells.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [10] Kolla N Wei Z Richardson JS Li XM Amitriptyline and fluoxetine protect PC12 cells from cell death induced by hydrogen peroxide Journal of Psychiatry and Neuroscience 2005 30 3 196 201 15944744 PMC1089780
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Individuals who suffer with MDD display lower serum/plasmatic total antioxidant potentials [28, 32, 48] and reduced brain GSH levels [31] as compared to matched controls.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 3. Oxidative Stress in Major Depressive Disorder
What the sources say
- Not checked yetcites [31] Gawryluk JW Wang JF Andreazza AC Shao L Young LT Decreased levels of glutathione, the major brain antioxidant, in post-mortem prefrontal cortex from patients with psychiatric disorders International Journal of Neuropsychopharmacology 2011 14 1 123 130 20633320 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Katyare and Rajan (1995) showed that long-term administration of imipramine to female rats resulted in significant stimulation of the states 3 and 4 respiration rates.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [20] Katyare SS Rajan RR Effect of long-term in vivo treatment with imipramine on the oxidative energy metabolism in rat brain mitochondria Comparative Biochemistry and Physiology Part C 1995 112 3 353 357 8838689
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The overall effects are more pronounced in the higher dose (24 versus 8 mg/kg) [22].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [22] Inkielewicz-Stêpniak I Impact of fluoxetine on liver damage in rats Pharmacological Reports 2011 63 2 441 447 21602599 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“pretreatment with imipramine, fluvoxamine, or reboxetine inhibited NO production in a dose-dependent manner in an activated microglia cell culture protocol [11].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [11] Hashioka S Klegeris A Monji A Antidepressants inhibit interferon-γ-induced microglial production of IL-6 and nitric oxide Experimental Neurology 2007 206 1 33 42 17481608 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Nortriptyline was able to inhibit loss of mitochondrial membrane potential and the activation of caspase 3 in isolated rat liver mitochondria”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [9] Zhang WH Wang H Wang X Nortriptyline protects mitochondria and reduces cerebral ischemia/hypoxia injury Stroke 2008 39 2 455 462 18174477 PMC2632945 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Abdel-Wahab and Salama (2011) showed that long-term venlafaxine treatment at effective antidepressant dosages can protect against stress-induced oxidative cellular and DNA damage in male mice.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [26] Abdel-Wahab BA Salama RH Venlafaxine protects against stress-induced oxidative DNA damage in hippocampus during antidepressant testing in mice Pharmacology Biochemistry and Behavior 2011 100 1 59 65 21835191 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, studies in vitro not only revealed antioxidant-related effects for antidepressant drugs, but also some potential prooxidant effects specifically in rat liver with fluoxetine at higher dosages.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The activities of alanine transaminase (ALT), aspartate transaminase (AST), and GST were increased in the serum.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [22] Inkielewicz-Stêpniak I Impact of fluoxetine on liver damage in rats Pharmacological Reports 2011 63 2 441 447 21602599 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Finally, this treatment was able to reduce serum and hippocampal levels of 8-OHdG (a marker of DNA damage) in stressed animals [26]”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [26] Abdel-Wahab BA Salama RH Venlafaxine protects against stress-induced oxidative DNA damage in hippocampus during antidepressant testing in mice Pharmacology Biochemistry and Behavior 2011 100 1 59 65 21835191 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“These results suggest that the effects of these antidepressants on the expression of antioxidant enzymes are dependent on the duration of the treatment regimen.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [12] Schmidt AJ Heiser P Hemmeter UM Krieg JC Vedder H Effects of antidepressants on mRNA levels of antioxidant enzymes in human monocytic U-937 cells Progress in Neuro-Psychopharmacology and Biological Psychiatry 2008 32 6 1567 1573 18573300 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“fluoxetine altered several markers of apoptosis in the liver, including decreased Bcl-2 expression and increased DNA fragmentation [25].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [25] Djordjevic J Djordjevic A Adzic M Elaković I Matić G Radojcic MB Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver European Journal of Pharmacology 2011 659 1 61 66 21414309 source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Curti et al. (1999) reported that fluoxetine can indirectly and nonspecifically affect electron transport and F1F0-ATPase activity, thereby inhibiting oxidative phosphorylation in rat brain [6].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [6] Curti C Mingatto FE Polizello ACM Galastri LO Uyemura SA Santos AC Fluoxetine interacts with the lipid bilayer of the inner membrane in isolated rat brain mitochondria, inhibiting electron transport and F1F0-ATPase activity Molecular and Cellular Biochemistry 1999 199 1-2 103 109 10544958 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, studies in vitro not only revealed antioxidant-related effects for antidepressant drugs, but also some potential prooxidant effects specifically in rat liver with fluoxetine at higher dosages.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Also, pretreatment with amitriptyline and fluoxetine was associated with increased SOD activity, and no signs of cell death were observed in the treated cells [10].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [10] Kolla N Wei Z Richardson JS Li XM Amitriptyline and fluoxetine protect PC12 cells from cell death induced by hydrogen peroxide Journal of Psychiatry and Neuroscience 2005 30 3 196 201 15944744 PMC1089780
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“short-term treatment with these drugs decreased mRNA levels of SOD and CAT.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [12] Schmidt AJ Heiser P Hemmeter UM Krieg JC Vedder H Effects of antidepressants on mRNA levels of antioxidant enzymes in human monocytic U-937 cells Progress in Neuro-Psychopharmacology and Biological Psychiatry 2008 32 6 1567 1573 18573300 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Chronic fluoxetine treatment increased the levels of TBARS, carbonyl groups, and the uric acid content in the liver.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [22] Inkielewicz-Stêpniak I Impact of fluoxetine on liver damage in rats Pharmacological Reports 2011 63 2 441 447 21602599 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“and decrease cell death induced by oxygen/glucose deprivation on PCN cells [9].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [9] Zhang WH Wang H Wang X Nortriptyline protects mitochondria and reduces cerebral ischemia/hypoxia injury Stroke 2008 39 2 455 462 18174477 PMC2632945 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Réus et al. (2010) reported increased SOD and CAT activity and decreased lipid and protein damage in male rat prefrontal cortex and hippocampus after both acute and chronic treatment with imipramine [17].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [17] Réus GZ Stringari RB De Souza B Harmine and imipramine promote antioxidant activities in prefrontal cortex and hippocampus Oxidative Medicine and Cellular Longevity 2010 3 5 325 331 21150338 PMC3154037 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, long-term treatment increased mRNA levels of SOD, GST, and GR.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [12] Schmidt AJ Heiser P Hemmeter UM Krieg JC Vedder H Effects of antidepressants on mRNA levels of antioxidant enzymes in human monocytic U-937 cells Progress in Neuro-Psychopharmacology and Biological Psychiatry 2008 32 6 1567 1573 18573300 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“They found that restraint stress significantly increased the generation of ROS in the peripheral blood”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [23] Novio S Núñez MJ Amigo G Freire-Garabal M Effects of fluoxetine on the oxidative status of peripheral blood leucocytes of restraint-stressed mice Basic & Clinical Pharmacology & Toxicology 2011 109 5 365 371 21624059 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, studies in animal models suggest that antidepressant agents modulate antioxidant enzyme activities and decrease oxidative stress markers on liver, brain, and peripheral tissues.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Along with antidepressant-like effects, long-term treatment with alpha-tocopherol enhanced antioxidant defences in the mouse hippocampus and prefrontal cortex, two structures closely implicated in the pathophysiology of depression [19].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [19] Lobato KR Cardoso CC Binfaré RW α-Tocopherol administration produces an antidepressant-like effect in predictive animal models of depression Behavioural Brain Research 2010 209 2 249 259 20144659 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In another study, plasmatic vitC levels were reduced in patients with MDD compared with age- and sex-matched healthy volunteers (n = 40).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [27] Khanzode SD Dakhale GN Khanzode SS Saoji A Palasodkar R Oxidative damage and major depression: the potential antioxidant action of selective serotonin-re-uptake inhibitors Redox Report 2003 8 6 365 370 14980069 source
plaincorrelationaln = 40- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The antioxidant effects of antidepressant drugs seem to vary depending on the dose, treatment regimen, and duration.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, while some changes in antioxidant enzymes have been observed in MDD, these post-mortem studies are not conclusive mostly because of small sample sizes, lack of control groups, and lack of relevant information (i.e., treatment duration, specific drugs used).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.3. Post-Mortem Studies
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“whereas chronic treatment increased GSH in both hippocampus and prefrontal cortex of female mice [19].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [19] Lobato KR Cardoso CC Binfaré RW α-Tocopherol administration produces an antidepressant-like effect in predictive animal models of depression Behavioural Brain Research 2010 209 2 249 259 20144659 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Notably, these antioxidant effects were persistent after 12 weeks of treatment [27].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [27] Khanzode SD Dakhale GN Khanzode SS Saoji A Palasodkar R Oxidative damage and major depression: the potential antioxidant action of selective serotonin-re-uptake inhibitors Redox Report 2003 8 6 365 370 14980069 source
plaindirectn = 62- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Two recent studies showed reduced oxidized and total GSH in the prefrontal cortex of MDD subjects as compared to controls [31, 36].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.3. Post-Mortem Studies
What the sources say
- Not checked yetcites [31] Gawryluk JW Wang JF Andreazza AC Shao L Young LT Decreased levels of glutathione, the major brain antioxidant, in post-mortem prefrontal cortex from patients with psychiatric disorders International Journal of Neuropsychopharmacology 2011 14 1 123 130 20633320 source
- Not checked yetcites [36] Gawryluk JW Wang JF Andreazza AC Shao L Yatham LN Young LT Prefrontal cortex glutathione S-transferase levels in patients with bipolar disorder, major depression and schizophrenia The International Journal of Neuropsychopharmacology 2011 14 8 1069 1074 21733244 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Also, fluoxetine and venlafaxine treatment prevented lipid and protein oxidative damage induced by stress [24].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [24] Zafir A Ara A Banu N In vivo antioxidant status: a putative target of antidepressant action Progress in Neuro-Psychopharmacology and Biological Psychiatry 2009 33 2 220 228 19059298 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The antidepressant-like effect of bupropion was prevented by pretreatment with L-arginine (a substrate of nitric oxide synthase, NOS).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [13] Dhir A Kulkarni SK Involvement of nitric oxide (NO) signaling pathway in the antidepressant action of bupropion, a dopamine reuptake inhibitor European Journal of Pharmacology 2007 568 1–3 177 185 17509558 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The antidepressant-like effect of escitalopram in the forced swim test (FST) was prevented by pretreatment with N-methyl-D-aspartic acid (NMDA), L-arginine, and sildenafil (a phosphodiesterase inhibitor).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [14] Zomkowski ADE Engel D Gabilan NH Rodrigues ALS Involvement of NMDA receptors and l-arginine-nitric oxide-cyclic guanosine monophosphate pathway in the antidepressant-like effects of escitalopram in the forced swimming test European Neuropsychopharmacology 2010 20 11 793 801 20810255 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“acute treatment with fluoxetine partially reversed this effect, possibly through normalization of SOD and CAT activity and GSH content [23].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [23] Novio S Núñez MJ Amigo G Freire-Garabal M Effects of fluoxetine on the oxidative status of peripheral blood leucocytes of restraint-stressed mice Basic & Clinical Pharmacology & Toxicology 2011 109 5 365 371 21624059 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Increased serum SOD and MDA levels have been found in a cohort of 62 major depressive patients (age 43.8 ± 12.9, mean ± SD; 34/28, female/male ratio) [27].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [27] Khanzode SD Dakhale GN Khanzode SS Saoji A Palasodkar R Oxidative damage and major depression: the potential antioxidant action of selective serotonin-re-uptake inhibitors Redox Report 2003 8 6 365 370 14980069 source
plainn = 62- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Consistent with the above-mentioned studies, changes in the blood/brain antioxidant profile have been associated with changes in depressive-like behaviour.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Also, the administration of 7-nitroindazole, methylene blue or ODQ (i.c.v., a soluble sGC inhibitor) in combination with escitalopram reduced the immobility time in the FST.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [14] Zomkowski ADE Engel D Gabilan NH Rodrigues ALS Involvement of NMDA receptors and l-arginine-nitric oxide-cyclic guanosine monophosphate pathway in the antidepressant-like effects of escitalopram in the forced swimming test European Neuropsychopharmacology 2010 20 11 793 801 20810255 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“More specifically, it has been demonstrated that some classic antioxidants induce antidepressant-like effects in rodents.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Overall, most animal and human data support that antidepressant drugs exert antioxidant effects during treatment for MDD.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“The results evidenced a significant recovery in the activities of SOD, CAT, GST, GR, and GSH levels by these antidepressants after restraint stress.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [24] Zafir A Ara A Banu N In vivo antioxidant status: a putative target of antidepressant action Progress in Neuro-Psychopharmacology and Biological Psychiatry 2009 33 2 220 228 19059298 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“These results suggest increased ROS production in brain samples of depressive patients due to increased XO activity.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.3. Post-Mortem Studies
What the sources say
- Not checked yetcites [35] Michel TM Camara S Tatschner T Increased xanthine oxidase in the thalamus and putamen in depression World Journal of Biological Psychiatry 2010 11 2 314 320 20218795 source
hedgeddirectn = 7- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Notably, a number of clinical trials revealed that treatment with antidepressants can reverse the increased oxidative stress observed in individuals with MDD.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In addition, treatment with methylene blue (a direct inhibitor of NOS and soluble guanylate cyclase, sGC) potentiated the effect of the drug in the forced swim test [13].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [13] Dhir A Kulkarni SK Involvement of nitric oxide (NO) signaling pathway in the antidepressant action of bupropion, a dopamine reuptake inhibitor European Journal of Pharmacology 2007 568 1–3 177 185 17509558 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In vitro and animal studies also suggest that some antidepressants may be prooxidant at high doses.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“These effects seemed to be associated with liver toxicity induced by high-dose fluoxetine treatment in rats.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [25] Djordjevic J Djordjevic A Adzic M Elaković I Matić G Radojcic MB Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver European Journal of Pharmacology 2011 659 1 61 66 21414309 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Additionally, alpha-tocopherol (vitamin E) administration produced antidepressant-like effects in animal models of depression.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [19] Lobato KR Cardoso CC Binfaré RW α-Tocopherol administration produces an antidepressant-like effect in predictive animal models of depression Behavioural Brain Research 2010 209 2 249 259 20144659 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Krass et al. (2011) reported that imipramine decreased brain nitrite + nitrate (NO2 + NO3) levels, a marker of nitrosative stress, in male rat brain.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [16] Vismari L Alves GJ Muscará MN Palermo-Neto J A possible role to nitric oxide in the anti-inflammatory effects of amitriptyline Immunopharmacology and Immunotoxicology. In press 22208160
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Short-term treatments (4 to 8 weeks) do not seem to alter antioxidant/oxidative parameters in MDD patients, whereas longer treatments (12 to 24 weeks) seem to induce robust antioxidant effects.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Corroborating with animal data, the majority of these studies revealed that antidepressant agents possess antioxidant properties when used in the treatment of MDD.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
plaindirectn = 62- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Findings from animal models and in vitro studies about antidepressant antioxidant effects are relevant to human MDD treatment.
- Rests on an assumption: Peripheral markers of oxidative stress (serum/plasmatic) reflect central/brain oxidative stress in MDD.
In the paper
“acute fluoxetine treatment reduced GPx activity in the hippocampus”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [19] Lobato KR Cardoso CC Binfaré RW α-Tocopherol administration produces an antidepressant-like effect in predictive animal models of depression Behavioural Brain Research 2010 209 2 249 259 20144659 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, there is a clear association between high dosages of antidepressants and increased hepatic oxidative stress.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“This study highlights the role of NMDA receptors and L-arginine-NO-cGMP pathway in the mechanism of action of antidepressant agents [14].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [14] Zomkowski ADE Engel D Gabilan NH Rodrigues ALS Involvement of NMDA receptors and l-arginine-nitric oxide-cyclic guanosine monophosphate pathway in the antidepressant-like effects of escitalopram in the forced swimming test European Neuropsychopharmacology 2010 20 11 793 801 20810255 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“This study suggests that bupropion possesses antidepressant-like activities in different animal models possibly through dopaminergic and L-arginine-NO-cyclic guanosine monophosphate (cGMP) signaling pathways.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [13] Dhir A Kulkarni SK Involvement of nitric oxide (NO) signaling pathway in the antidepressant action of bupropion, a dopamine reuptake inhibitor European Journal of Pharmacology 2007 568 1–3 177 185 17509558 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“This antidepressant-like effect of Ginkgo biloba extract was associated with a reduction in lipid peroxidation and superoxide radical production (as indicated by a downregulation of SOD activity) [54].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [54] Rojas P Serrano-García N Medina-Campos ON Pedraza-Chaverri J Ögren SO Rojas C Antidepressant-like effect of a Ginkgo biloba extract (EGb761) in the mouse forced swimming test: role of oxidative stress Neurochemistry International 2011 59 5 628 638 21672588 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Oxidative stress markers (SOD, vitC, lipid peroxidation) were reversed after 4 weeks of treatment with fluoxetine (20 mg/day, n = 32) and citalopram (20 mg/day, n = 30).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [27] Khanzode SD Dakhale GN Khanzode SS Saoji A Palasodkar R Oxidative damage and major depression: the potential antioxidant action of selective serotonin-re-uptake inhibitors Redox Report 2003 8 6 365 370 14980069 source
plaindirectn = 32- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In addition, GPx levels were reduced in MDD subjects [31].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.3. Post-Mortem Studies
What the sources say
- Not checked yetcites [31] Gawryluk JW Wang JF Andreazza AC Shao L Young LT Decreased levels of glutathione, the major brain antioxidant, in post-mortem prefrontal cortex from patients with psychiatric disorders International Journal of Neuropsychopharmacology 2011 14 1 123 130 20633320 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Short-term treatments (4 to 8 weeks) do not seem to alter antioxidant/oxidative parameters in MDD patients, whereas longer treatments (12 to 24 weeks) seem to induce robust antioxidant effects.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Pretreatment with 7-nitroindazole (a specific neuronal NO synthase, nNOS inhibitor) potentiated bupropion's effects.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [13] Dhir A Kulkarni SK Involvement of nitric oxide (NO) signaling pathway in the antidepressant action of bupropion, a dopamine reuptake inhibitor European Journal of Pharmacology 2007 568 1–3 177 185 17509558 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“This result supports the idea that antidepressants are able to inhibit NO synthesis in the rat brain [16]”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [16] Vismari L Alves GJ Muscará MN Palermo-Neto J A possible role to nitric oxide in the anti-inflammatory effects of amitriptyline Immunopharmacology and Immunotoxicology. In press 22208160
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“In one study, treatment with Ginkgo biloba extract (10 mg/kg) reduced recorded immobility time in the forced swimming test (FST) to the same extent as imipramine (39% versus 38%).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [54] Rojas P Serrano-García N Medina-Campos ON Pedraza-Chaverri J Ögren SO Rojas C Antidepressant-like effect of a Ginkgo biloba extract (EGb761) in the mouse forced swimming test: role of oxidative stress Neurochemistry International 2011 59 5 628 638 21672588 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“there is increasing body of evidence supporting that MDD may be associated with changes in oxidative stress markers”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“and MDA levels were positively correlated with the severity of MDD.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [33] Kotan VO Sarandol E Kirhan E Ozkaya G Kirli S Effects of long-term antidepressant treatment on oxidative status in major depressive disorder: a 24-week follow-up study Progress in Neuro-Psychopharmacology and Biological Psychiatry 2011 35 5 1284 1290 21515329 source
plaincorrelationaln = 50- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and that antidepressant agents (especially long-term treatment) may increase antioxidant defences.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“After treatment with four different SSRIs drugs (fluoxetine 20 mg/day, n = 7; sertraline 50 mg/day, n = 13; fluvoxamine 100 mg/day, n = 5; or citalopram 20 mg/day, n = 5), for 12 weeks, antioxidant enzyme activities (plasmatic GPx) and MDA levels (plasma and erythrocyte) were restored to control levels.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [30] Bilici M Efe H Köroğlu MA Uydu HA Bekaroğlu M Değer O Antioxidative enzyme activities and lipid peroxidation in major depression: alterations by antidepressant treatments Journal of Affective Disorders 2001 64 1 43 51 11292519 source
plaindirectn = 32- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Overall, the literature reviewed does not support differences in antioxidant potential between different antidepressant agents/classes.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Sarandol et al. (2007) found that MDD was accompanied by increased peripheral oxidative stress”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [28] Sarandol A Sarandol E Eker SS Erdinc S Vatansever E Kirli S Major depressive disorder is accompanied with oxidative stress: short-term antidepressant treatment does not alter oxidative—antioxidative systems Human Psychopharmacology 2007 22 2 67 73 17299810 source
plaincorrelationaln = 96- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“After three months of fluoxetine treatment, MDA levels were normalized [48].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [48] Gałecki P Szemraj J Bieńkiewicz M Florkowski A Gałecka E Lipid peroxidation and antioxidant protection in patients during acute depressive episodes and in remission after fluoxetine treatment Pharmacological Reports 2009 61 3 436 447 19605942 source
plaindirectn = 50- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“indicating that the oxidative stress observed in depressed patients was partly improved during 24 weeks of antidepressant treatment.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
hedgeddirectn = 50- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These further suggest that recovery from a major depressive episode may be associated with normalization of antioxidant potential induced by antidepressants.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
hedgedcorrelationaln = 57- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“After 24-weeks of treatment, MDA and SOD levels decreased.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [33] Kotan VO Sarandol E Kirhan E Ozkaya G Kirli S Effects of long-term antidepressant treatment on oxidative status in major depressive disorder: a 24-week follow-up study Progress in Neuro-Psychopharmacology and Biological Psychiatry 2011 35 5 1284 1290 21515329 source
plaindirectn = 50- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Plasmatic GR and erythrocyte SOD were also significantly decreased in MD patients after 12-week antidepressant treatment [30].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [30] Bilici M Efe H Köroğlu MA Uydu HA Bekaroğlu M Değer O Antioxidative enzyme activities and lipid peroxidation in major depression: alterations by antidepressant treatments Journal of Affective Disorders 2001 64 1 43 51 11292519 source
plaindirectn = 32- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Brain imaging studies have suggested that MDD may be associated with decreased volumes of various brain regions [58–60].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
What the sources say
- Not checked yetcites [58] Stockmeier CA Mahajan GJ Konick LC Cellular changes in the postmortem hippocampus in major depression Biological Psychiatry 2004 56 9 640 650 15522247 PMC2929806 source
- Not checked yetcites [59] Zou K Deng W Li T Changes of brain morphometry in first-episode, drug-Naïve, non-late-life adult patients with major depression: an optimized voxel-based morphometry study Biological Psychiatry 2010 67 2 186 188 19897176 source
- Not checked yetcites [60] Campbell S MacQueen G An update on regional brain volume differences associated with mood disorders Current Opinion in Psychiatry 2006 19 1 25 33 16612175 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“TOS and OSI were higher and TAC level was lower in the MDD group compared with controls (n = 40).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [32] Cumurcu BE Ozyurt H Etikan I Demir S Karlidag R Total antioxidant capacity and total oxidant status in patients with major depression: impact of antidepressant treatment Psychiatry and Clinical Neurosciences 2009 63 5 639 645 19674383 source
plaincorrelationaln = 40- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, TAC was also found decreased after 24-week treatment with antidepressants”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [33] Kotan VO Sarandol E Kirhan E Ozkaya G Kirli S Effects of long-term antidepressant treatment on oxidative status in major depressive disorder: a 24-week follow-up study Progress in Neuro-Psychopharmacology and Biological Psychiatry 2011 35 5 1284 1290 21515329 source
plaindirectn = 50- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“many of these studies were short in duration and likely underpowered to address the question of differences in antioxidant potential amongst particular drugs”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Patients on venlafaxine were also compared with patients on SSRIs in the aspect of oxidative stress parameters in the follow-up period, but no significant differences were found [33].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [33] Kotan VO Sarandol E Kirhan E Ozkaya G Kirli S Effects of long-term antidepressant treatment on oxidative status in major depressive disorder: a 24-week follow-up study Progress in Neuro-Psychopharmacology and Biological Psychiatry 2011 35 5 1284 1290 21515329 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Plasmatic CoQ10 was lower in depressed patients than controls.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [34] Maes M Mihaylova I Kubera M Uytterhoeven M Vrydags N Bosmans E Lower plasma Coenzyme Q10 in depression: a marker for treatment resistance and chronic fatigue in depression and a risk factor to cardiovascular disorder in that illness Neuroendocrinology Letters 2009 30 4 462 469 20010493
plaincorrelationaln = 35- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Also, the authors did not find a significant relationship between the duration of illness and SOD, XO activities, or nitrite levels in this cohort.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [29] Herken H Gurel A Selek S Adenosine deaminase, nitric oxide, superoxide dismutase, and xanthine oxidase in patients with major depression: impact of antidepressant treatment Archives of Medical Research 2007 38 2 247 252 17227736 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“An important issue in biomarker research is the fact that peripheral markers may not necessarily correlate with changes in the central nervous system.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Presence of temporal lobe atrophy and moderate-to-severe white matter lesions can predict occurrence of major depression during a 5-year followup in a population-based sample of elderly [62].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
What the sources say
- Not checked yetcites [62] Olesen PJ Gustafson DR Simoni M Temporal lobe atrophy and white matter lesions are related to major depression over 5 years in the elderly Neuropsychopharmacology 2010 35 13 2638 2645 20881949 PMC3055580 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Also, a negative correlation was found between the severity of the disease and serum TAC (r = −0.553) at the pretreatment stage.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [32] Cumurcu BE Ozyurt H Etikan I Demir S Karlidag R Total antioxidant capacity and total oxidant status in patients with major depression: impact of antidepressant treatment Psychiatry and Clinical Neurosciences 2009 63 5 639 645 19674383 source
plaincorrelationaln = 57- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“After 3 months of treatment with escitalopram, 10–20 mg/day, n = 10; paroxetine, 20–40 mg/day, n = 20; or sertraline, 50–100 mg/day, n = 27, TOS and OSI were decreased and TAC was increased compared with pretreatment values [32].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [32] Cumurcu BE Ozyurt H Etikan I Demir S Karlidag R Total antioxidant capacity and total oxidant status in patients with major depression: impact of antidepressant treatment Psychiatry and Clinical Neurosciences 2009 63 5 639 645 19674383 source
plaindirectn = 57- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Decreased serum SOD and increased XO were found in 20 individuals with MDD (age range 17–62 years, 19/17 F/M ratio) [29].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [29] Herken H Gurel A Selek S Adenosine deaminase, nitric oxide, superoxide dismutase, and xanthine oxidase in patients with major depression: impact of antidepressant treatment Archives of Medical Research 2007 38 2 247 252 17227736 source
plaincorrelationaln = 20- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“MDD subjects have smaller normalized frontal lobe volumes when compared with the nondepressed controls after controlling for age, gender and “total cumulative illness rating scale score” [61].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
What the sources say
- Not checked yetcites [61] Kumar A Bilker W Jin Z Udupa J Atrophy and high intensity lesions: complementary neurobiological mechanisms in late-life major depression Neuropsychopharmacology 2000 22 3 264 274 10693154 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Bilici et al. (2001) reported increased oxidative stress in major depressive patients (n = 32), indexed by higher antioxidant enzyme activities (erythrocyte SOD, GPx, and plasmatic GR) and MDA levels (erythrocyte and plasmatic).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [30] Bilici M Efe H Köroğlu MA Uydu HA Bekaroğlu M Değer O Antioxidative enzyme activities and lipid peroxidation in major depression: alterations by antidepressant treatments Journal of Affective Disorders 2001 64 1 43 51 11292519 source
plaincorrelationaln = 32- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“however, short-term antidepressant treatment (6 weeks) did not alter oxidative/antioxidant systems in a cohort of 96 MDD patients (age 40 ± 11, 72/24 F/M ratio).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [28] Sarandol A Sarandol E Eker SS Erdinc S Vatansever E Kirli S Major depressive disorder is accompanied with oxidative stress: short-term antidepressant treatment does not alter oxidative—antioxidative systems Human Psychopharmacology 2007 22 2 67 73 17299810 source
plainn = 96- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It is possible that augmentation of antioxidant defences may be one of the mechanisms underlying the neuroprotective effects of antidepressants observed in the treatment of MDD.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Peripheral biomarkers detected during acute mood episodes could in fact constitute markers of disease activity [68].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
What the sources say
- Not checked yetcites [68] Kapczinski F Dal-Pizzol F Teixeira AL A systemic toxicity index developed to assess peripheral changes in mood episodes Molecular Psychiatry 2010 15 8 784 786 20351717 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“After 6 weeks of treatment with venlafaxine 75–150 mg/day, sertraline 50 mg/day, or reboxetine 4–8 mg/day, these oxidative parameters were not altered [28].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [28] Sarandol A Sarandol E Eker SS Erdinc S Vatansever E Kirli S Major depressive disorder is accompanied with oxidative stress: short-term antidepressant treatment does not alter oxidative—antioxidative systems Human Psychopharmacology 2007 22 2 67 73 17299810 source
plainn = 96- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“suggesting that normalization of these enzymes was associated with symptomatic improvement [29].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [29] Herken H Gurel A Selek S Adenosine deaminase, nitric oxide, superoxide dismutase, and xanthine oxidase in patients with major depression: impact of antidepressant treatment Archives of Medical Research 2007 38 2 247 252 17227736 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Teyssier et al. (2011) demonstrated that the expression of oxidative stress-response genes was not altered in the prefrontal cortex of individuals with MDD.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
What the sources say
- Not checked yetcites [65] Teyssier JR Ragot S Chauvet-Gélinier JC Trojak B Bonin B Expression of oxidative stress-response genes is not activated in the prefrontal cortex of patients with depressive disorder Psychiatry Research 2011 186 2-3 244 247 20800905 source
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“However, there was no correlation between plasma CoQ10 and the severity of illness or the number of depressive episodes.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [34] Maes M Mihaylova I Kubera M Uytterhoeven M Vrydags N Bosmans E Lower plasma Coenzyme Q10 in depression: a marker for treatment resistance and chronic fatigue in depression and a risk factor to cardiovascular disorder in that illness Neuroendocrinology Letters 2009 30 4 462 469 20010493
plainn = 35- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“There were no differences in plasma CoQ10 between depressed patients who were taking antidepressants and those without [34].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [34] Maes M Mihaylova I Kubera M Uytterhoeven M Vrydags N Bosmans E Lower plasma Coenzyme Q10 in depression: a marker for treatment resistance and chronic fatigue in depression and a risk factor to cardiovascular disorder in that illness Neuroendocrinology Letters 2009 30 4 462 469 20010493
plainn = 35- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 24
- Probably not a substantial claim. 2
- The quote only partly states this claim. 2
None of the sources cited for this claim have been checked yet.
In the paper
“The pathophysiology of depression is multifactorial and includes changes in brain monoaminergic transmission (e.g., 5-HT, NE, DA), abnormalities in neurotransmitter receptors function (e.g., AC-cAMP pathway), reduced neurotrophic factors (e.g., BDNF), dysregulation of HPA axis (cortisol), increased proinflammatory cytokines (e.g., IL-6, TNF-α, NF-κB), increased NO (e.g., L-arginine-NO-cGMP pathway”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 3. Oxidative Stress in Major Depressive Disorder
What the sources say
- Not checked yetcites [45] Coyle JT Puttfarcken P Oxidative stress, glutamate, and neurodegenerative disorders Science 1993 262 5134 689 695 7901908 source
- Not checked yetcites [46] Gardner A Boles RG Beyond the serotonin hypothesis: mitochondria, inflammation and neurodegeneration in major depression and affective spectrum disorders Progress in Neuro-Psychopharmacology and Biological Psychiatry 2011 35 3 730 743 20691744 source
- Not checked yetcites [47] Chopra K Kumar B Kuhad A Pathobiological targets of depression Expert Opinion on Therapeutic Targets 2011 15 4 379 400 21254923 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Dimopoulos et al. (2008) have found that F2-isoprostanes (F2-iso) circulatory levels were increased in major depressive patients and were significantly correlated with the severity of depressive symptoms [50].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 3. Oxidative Stress in Major Depressive Disorder
What the sources say
- Not checked yetcites [50] Dimopoulos N Piperi C Psarra V Lea RW Kalofoutis A Increased plasma levels of 8-iso-PGF2α and IL-6 in an elderly population with depression Psychiatry Research 2008 161 1 59 66 18783834 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“These results suggest that imipramine treatment may induce changes in substrate oxidation pattern, increase rate of ATP synthesis, and can potentially increase mitochondrial ROS production.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [20] Katyare SS Rajan RR Effect of long-term in vivo treatment with imipramine on the oxidative energy metabolism in rat brain mitochondria Comparative Biochemistry and Physiology Part C 1995 112 3 353 357 8838689
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“High dose (10 mg/kg) of venlafaxine, however, decreased the intensity of BDNF immunostaining in all subareas of the hippocampus and increased the intensity of Cu/Zn-SOD immunostaining in the dentate granular cell layer [21].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [21] Xu H Steven Richardson J Li XM Dose-related effects of chronic antidepressants on neuroprotective proteins BDNF, Bcl-2 and Cu/Zn-SOD in rat hippocampus Neuropsychopharmacology 2003 28 1 53 62 12496940 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Souza et al. (1994) reported that fluoxetine may be potentially hepatotoxic at high doses [7].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [7] Souza MEJ Polizello ACM Uyemura SA Castro-Silva O Curti C Effect of fluoxetine on rat liver mitochondria Biochemical Pharmacology 1994 48 3 535 541 8068040 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“low dose (5 mg/kg) of amitriptyline and venlafaxine increased the intensity of BDNF immunostaining in hippocampal pyramidal neurons and the intensity of Bcl-2 immunostaining in hippocampal mossy fibers, but did not alter the Cu/Zn-SOD immunoreactivity.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [21] Xu H Steven Richardson J Li XM Dose-related effects of chronic antidepressants on neuroprotective proteins BDNF, Bcl-2 and Cu/Zn-SOD in rat hippocampus Neuropsychopharmacology 2003 28 1 53 62 12496940 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“At all doses tested, venlafaxine decreased MDA and total nitrite levels, increased total antioxidant potential and GSH content, and restored GST activity in hippocampus of stressed animals.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [26] Abdel-Wahab BA Salama RH Venlafaxine protects against stress-induced oxidative DNA damage in hippocampus during antidepressant testing in mice Pharmacology Biochemistry and Behavior 2011 100 1 59 65 21835191 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Nahon et al. (2005) demonstrated that fluoxetine was able to inhibit the opening of the mitochondrial permeability transition (MPT) pore, the release of cytochrome c (cytC) and protected against staurosporine-induced apoptotic cell death [8].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.1. Studies In Vitro
What the sources say
- Not checked yetcites [8] Nahon E Israelson A Abu-Hamad S Shoshan-Barmatz V Fluoxetine (Prozac) interaction with the mitochondrial voltage-dependent anion channel and protection against apoptotic cell death FEBS Letters 2005 579 22 5105 5110 16139271 source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Venlafaxine also promoted increased total antioxidant potential and GSH levels in the control, nonstressed group.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [26] Abdel-Wahab BA Salama RH Venlafaxine protects against stress-induced oxidative DNA damage in hippocampus during antidepressant testing in mice Pharmacology Biochemistry and Behavior 2011 100 1 59 65 21835191 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Control animals and stressed animals displayed decreased activity of SOD and increased activity of GPx.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [25] Djordjevic J Djordjevic A Adzic M Elaković I Matić G Radojcic MB Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver European Journal of Pharmacology 2011 659 1 61 66 21414309 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one. The quote only partly states this claim.
In the paper
“Djordjevic et al. (2011) showed altered antioxidant status and increased apoptotic signalling in male rat liver after 21 days of fluoxetine treatment.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [25] Djordjevic J Djordjevic A Adzic M Elaković I Matić G Radojcic MB Fluoxetine affects antioxidant system and promotes apoptotic signaling in Wistar rat liver European Journal of Pharmacology 2011 659 1 61 66 21414309 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Additionally, imipramine treatment increased brain creatine kinase and increased activity of mitochondrial respiratory chain complexes [18, 53].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [18] Reus GZ Stringari RB Gonçalves CL Administration of harmine and imipramine alters creatine kinase and mitochondrial respiratory chain activities in the rat brain Depression Research and Treatment 2012 2012 7 pages Article ID 987397. PMC3182396 21969912
- Not checked yetcites [53] Reus GZ Stringari RB Rezin GT Administration of memantine and imipramine alters mitochondrial respiratory chain and creatine kinase activities in rat brain Journal of Neural Transmission 2012 119 4 481 491 21953515 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one), a substance that mimics the activity of the antioxidant enzyme GPx [56], decreased immobility time in rodents, an effect that was dependent on its interaction with the noradrenergic and dopaminergic systems [57].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [57] Posser T Kaster MP Baraúna SC Rocha JBT Rodrigues ALS Leal RB Antidepressant-like effect of the organoselenium compound ebselen in mice: evidence for the involvement of the monoaminergic system European Journal of Pharmacology 2009 602 1 85 91 19026628 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In rats displaying depressive-like behaviour induced by chronic mild stress, administration of liquiritin, an antioxidant derived from Glycyrrhiza uralensis, decreased immobility time, increased sucrose consumption, increased SOD activity, and attenuated MDA production in the peripheral blood [55].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [55] Zhao Z Wang W Guo H Zhou D Antidepressant-like effect of liquiritin from Glycyrrhiza uralensis in chronic variable stress induced depression model rats Behavioural Brain Research 2008 194 1 108 113 18655806 source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In a subsequent study with the same cohort, GST levels were also reduced in MDD patients and no effects of antidepressant treatment were observed [36].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.3. Post-Mortem Studies
What the sources say
- Not checked yetcites [36] Gawryluk JW Wang JF Andreazza AC Shao L Yatham LN Young LT Prefrontal cortex glutathione S-transferase levels in patients with bipolar disorder, major depression and schizophrenia The International Journal of Neuropsychopharmacology 2011 14 8 1069 1074 21733244 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, a major limitation of the studies above mentioned is that not all studies measured oxidative stress markers (i.e., MDA, carbonyl); therefore, these prooxidant effects need further investigation.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“No differences in locomotor activity were observed, suggesting a selective antidepressant-like effect.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 4. Antioxidant Effects of Antidepressants > 4.2. Animal Models
What the sources say
- Not checked yetcites [54] Rojas P Serrano-García N Medina-Campos ON Pedraza-Chaverri J Ögren SO Rojas C Antidepressant-like effect of a Ginkgo biloba extract (EGb761) in the mouse forced swimming test: role of oxidative stress Neurochemistry International 2011 59 5 628 638 21672588 source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Plasmatic MDA, serum oxidized LDL (OxLDL) levels, and erythrocyte SOD activity were increased in MDD patients before treatment”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [33] Kotan VO Sarandol E Kirhan E Ozkaya G Kirli S Effects of long-term antidepressant treatment on oxidative status in major depressive disorder: a 24-week follow-up study Progress in Neuro-Psychopharmacology and Biological Psychiatry 2011 35 5 1284 1290 21515329 source
plainn = 50- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“there is also evidence suggesting that BDNF, oxidative stress, and inflammation tend to be abnormal among individuals with multiple mood episodes and correlate with length of illness [51, 66, 67].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
What the sources say
- Not checked yetcites [51] Praticò D Rokach J Lawson J FitzGerald GA F2-isoprostanes as indices of lipid peroxidation in inflammatory diseases Chemistry and Physics of Lipids 2004 128 1-2 165 171 15037161 source
- Not checked yetcites [66] Frey BN Zunta-Soares GB Caetano SC Illness duration and total brain gray matter in bipolar disorder: evidence for neurodegeneration? European Neuropsychopharmacology 2008 18 10 717 722 18554875 source
- Not checked yetcites [67] Minuzzi L Behr GA Moreira JCF Frey BN Mitochondrial dysfunction in bipolar disorder: lessons from brain imaging and molecular markers Revista Colombiana de Psiquiatría 2011 40 166 182 source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Considering that the presence of oxidative (and nitrosative) stress may cause neurodegeneration and reduced neurogenesis [63, 64]”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
What the sources say
- Not checked yetcites [63] Maes M Ruckoanich P Chang YS Mahanonda N Berk M Multiple aberrations in shared inflammatory and oxidative & nitrosative stress (IO&NS) pathways explain the co-association of depression and cardiovascular disorder (CVD), and the increased risk for CVD and due mortality in depressed patients Progress in Neuro-Psychopharmacology and Biological Psychiatry 2011 35 3 769 783 20561554 source
- Not checked yetcites [64] Maes M Galecki P Chang YS Berk M A review on the oxidative and nitrosative stress (O&NS) pathways in major depression and their possible contribution to the (neuro)degenerative processes in that illness Progress in Neuro-Psychopharmacology and Biological Psychiatry 2011 35 3 676 692 20471444 source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, in this post-mortem study all of the patients had received antidepressant treatment, which may have normalized oxidative stress parameters.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Also, SOD activity was increased in patients with MDD, and there was a positive correlation between the severity of depressive symptoms and SOD activity (r = 0.419).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [28] Sarandol A Sarandol E Eker SS Erdinc S Vatansever E Kirli S Major depressive disorder is accompanied with oxidative stress: short-term antidepressant treatment does not alter oxidative—antioxidative systems Human Psychopharmacology 2007 22 2 67 73 17299810 source
plaincorrelationaln = 96- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In this study, MDD patients had increased plasmatic MDA levels and increased susceptibility of red blood cells (RBCs) to oxidation.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [28] Sarandol A Sarandol E Eker SS Erdinc S Vatansever E Kirli S Major depressive disorder is accompanied with oxidative stress: short-term antidepressant treatment does not alter oxidative—antioxidative systems Human Psychopharmacology 2007 22 2 67 73 17299810 source
plaincorrelationaln = 96- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Furthermore, the authors found a positive correlation between the severity of the disease and serum TOS and OSI (r = 0.58, and r = 0.63, resp.).”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [32] Cumurcu BE Ozyurt H Etikan I Demir S Karlidag R Total antioxidant capacity and total oxidant status in patients with major depression: impact of antidepressant treatment Psychiatry and Clinical Neurosciences 2009 63 5 639 645 19674383 source
plaincorrelationaln = 57- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The quote only partly states this claim.
In the paper
“Before treatment, MDD patients displayed increased erythrocyte SOD and CAT activities, increased MDA levels, and decreased plasmatic total antioxidant status (TAS) level.”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [48] Gałecki P Szemraj J Bieńkiewicz M Florkowski A Gałecka E Lipid peroxidation and antioxidant protection in patients during acute depressive episodes and in remission after fluoxetine treatment Pharmacological Reports 2009 61 3 436 447 19605942 source
plainn = 50- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Treatment with citalopram (20 mg/day, n = 10), fluoxetine (20 mg/day, n = 11), fluvoxamine (150 mg/day, n = 7), or sertraline (50 mg/day, n = 8) for 8 weeks increased SOD activity whereas decreased XO levels”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
What the sources say
- Not checked yetcites [29] Herken H Gurel A Selek S Adenosine deaminase, nitric oxide, superoxide dismutase, and xanthine oxidase in patients with major depression: impact of antidepressant treatment Archives of Medical Research 2007 38 2 247 252 17227736 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“They concluded that the pathogenic role of oxidative stress in the neurobiology of depression could not be inferred from alterations in the periphery [65].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 6. Concluding Remarks
What the sources say
- Not checked yetcites [65] Teyssier JR Ragot S Chauvet-Gélinier JC Trojak B Bonin B Expression of oxidative stress-response genes is not activated in the prefrontal cortex of patients with depressive disorder Psychiatry Research 2011 186 2-3 244 247 20800905 source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
The paper relies on this without support.
Findings from animal models and in vitro studies about antidepressant antioxidant effects are relevant to human MDD treatment.
“This paper examines preclinical (in vitro and animal model) and clinical literature on oxidative/antioxidant effects associated with antidepressant agents and discusses their potential antioxidant-related effects in the treatment of MDD.”
The paper relies on this without support.
Peripheral markers of oxidative stress (serum/plasmatic) reflect central/brain oxidative stress in MDD.
“Individuals who suffer with MDD display lower serum/plasmatic total antioxidant potentials [28, 32, 48] and reduced brain GSH levels [31] as compared to matched controls.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“it was shown that the mood stabilizers and antidepressant therapies possess high antioxidant potential [115].”
From Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches (2016) · cites this paper as [115]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“Decreased serum SOD and increased XO were found in 20 individuals with MDD (age range 17–62 years, 19/17 F/M ratio) [29].”
§ Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder > 5. Clinical Data: Human Studies
Reported 20 · recomputed 36
Citations
Cites
Ellman, G. L. (1959) · Archives of Biochemistry and Biophysics · doi:10.1016/0003-9861(59)90090-6 · Cited by 26,824
Free radicals and antioxidants in normal physiological functions and human disease
Valko, M., Leibfritz, D., Moncol, J., Cronin, M. T. D., Mazur, M., & Telser, J. (2007) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2006.07.001 · Cited by 14,269
Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies
Lang, U. E., & Borgwardt, S. (2013) · Cellular Physiology and Biochemistry · doi:10.1159/000350094 · Cited by 8,526
Oxidative Stress, Glutamate, and Neurodegenerative Disorders
Coyle, J. T., & Puttfarcken, P. (1993) · Science · doi:10.1126/science.7901908 · Cited by 3,762
Rio, D. D., Stewart, A. J., & Pellegrini, N. (2005) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2005.05.003 · Cited by 2,789
Janero, D. R. (1990) · Free Radical Biology and Medicine · doi:10.1016/0891-5849(90)90131-2 · Cited by 2,735
Oxidative stress and neurodegeneration: where are we now?
Halliwell, B. (2006) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2006.03907.x · Cited by 2,614
Protein carbonyl groups as biomarkers of oxidative stress
Dalle‐Donne, I., Rossi, R., Giustarini, D., Milzani, A., & Colombo, R. (2003) · Clinica Chimica Acta · doi:10.1016/s0009-8981(03)00003-2 · Cited by 2,352
Biochemistry of oxidative stress
Halliwell, B. B. (2007) · Biochemical Society Transactions · doi:10.1042/bst0351147 · Cited by 1,591
Cellular Defenses against Superoxide and Hydrogen Peroxide
Imlay, J. A. (2008) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.77.061606.161055 · Cited by 1,563
Research works printed but not linked: 5
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- 2012, Depression Research and Treatment, 2012
- 1995, Comparative Biochemistry and Physiology Part C, 112, 353
- 2009, Neuroendocrinology Letters, 30, 462
- 2009, Neuroendocrinology Letters, 30, 715
Cited by
Sorted by citations
Oxidative Stress and the Central Nervous System
Salim, S. (2016) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.116.237503 · Cited by 1,268
Role of oxidative stress in depression
Bhatt, S., Nagappa, A. N., & Patil, C. R. (2020) · Drug Discovery Today · doi:10.1016/j.drudis.2020.05.001 · Cited by 854
Is depression associated with increased oxidative stress? A systematic review and meta-analysis
Black, C. N., Bot, M., Scheffer, P. G., Cuijpers, P., & Penninx, B. W. J. H. (2015) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2014.09.025 · Cited by 711
Oxidative Stress and Psychological Disorders
Salim, S. (2014) · Current Neuropharmacology · doi:10.2174/1570159x11666131120230309 · Cited by 557
Oxidative stress, inflammation and treatment response in major depression
Lindqvist, D., Dhabhar, F. S., James, S. J., Hough, C. M., Jain, F. A., Bersani, F. S., Reus, V. I., Verhoeven, J. E., Epel, E. S., Mahan, L., et al. (2017) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2016.11.031 · Cited by 473
Metadata
- Authors
- Behr, G. A., Moreira, J. C. F., & Frey, B. N.
- Affiliations
- Universidade Federal do Rio Grande do Sul (BR)
- McMaster University (CA)
- Corresponding author
- Behr, Guilherme A.
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2012
- Volume
- 2012
- Pages
- 1-13
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- PMC
- PMC3368202
- OpenAlex
- W1977657096
- Semantic Scholar
- 8844560d54d30597299b29b489c8ee918eb74996
- Cited by
- 205
- References
- 69
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 16 · 2023: 10 · 2022: 14 · 2021: 12 · 2020: 18 · 2019: 10 · 2018: 12 · 2017: 20 · 2016: 17 · 2015: 24 · 2014: 17 · 2013: 16 · 2012: 3
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (BEX 5383/10-2)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- major depressive disorder, antidepressants, antioxidant activity, oxidative stress, glutathione, F2-isoprostanes, 8-hydroxy-2'-deoxyguanosine, oxidative DNA damage, neuroprotection, antioxidant defense, antidepressant mechanism
- MeSH terms
- Animals, Antidepressive Agents, Antioxidants, Brain, Clinical Trials as Topic, Major Depressive Disorder, Depressive Disorder, Major, Disease Models, Animal, Drug Evaluation, Preclinical, Humans, Oxidative Stress
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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