Cited by 183Treatment of Major DepressionAntioxidant Activity and Oxidative StressTryptophan and brain disorders

In vivo antioxidant status: A putative target of antidepressant action

Zafir, Ayesha, Ara, Anjum, Banu, Naheed·2009·Progress in Neuro-Psychopharmacology and Biological Psychiatry

Abstract

Oxidative stress is a critical route of damage in various psychological stress-induced disorders, such as depression. Antidepressants are widely prescribed to treat these conditions; however, few animal studies have investigated the effect of these drugs on endogenous antioxidant status in the brain. The present study employed a 21-day chronic regimen of random exposure to restraint stress to induce oxidative stress in brain, and behavioural aberrations, in rodents. The forced swimming (FST) and sucrose preference tests were used to identify depression-like phenotypes, and reversal in these indices indicated the effectiveness of treatment with fluoxetine (FLU; 20 mg/kg/day, p.o.; selective serotonin reuptake inhibitor), imipramine (IMI; 10 mg/kg/day, p.o.; tricyclic antidepressant) and venlafaxine (VEN; 10 mg/kg/day, p.o.; dual serotonin/norepinephrine reuptake inhibitor) following restraint stress. The antioxidant status was investigated in the brain of these animals. The results evidenced a significant recovery in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), glutathione reductase (GR) and glutathione (GSH) levels by antidepressant treatments following a restraint stress-induced decline of these parameters. The severely accumulated lipid peroxidation product malondialdehyde (MDA) and protein carbonyl contents in stressed animals were significantly normalized by antidepressant treatments. The altered oxidative status is implicated in various aspects of cellular function affecting the brain. Thus, it is possible that augmentation of in vivo antioxidant defenses could serve as a convergence point for multiple classes of antidepressants as an important mechanism underlying the neuroprotective pharmacological effects of these drugs observed clinically in the treatment of various stress disorders. Consequently, pharmacological modulation of stress-induced oxidative damage as a possible stress-management approach should be an important avenue of further research.

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Crossref · 10.1016/j.pnpbp.2008.11.010

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Authors
Zafir, A., Ara, A., & Banu, N.
Affiliations
Aligarh Muslim University (IN)
Corresponding author
Banu, Naheed
Venue
Progress in Neuro-Psychopharmacology and Biological Psychiatry
Publisher
Elsevier BV
Published
2009-03
Volume
33
Issue
2
Pages
220-228
ISSN
0278-5846 (ISSN-L)
OpenAlex
W2074602237
Cited by
183
References
84
Citations by year
2026: 2 · 2025: 4 · 2024: 5 · 2023: 5 · 2022: 7 · 2021: 8 · 2020: 7 · 2019: 7 · 2018: 6 · 2017: 15 · 2016: 15 · 2015: 13 · 2014: 20 · 2013: 15 · 2012: 17
FWCI
8.66
Type
journal article
Language
en
Open access
closed
Locations
  • Progress in Neuro-Psychopharmacology and Biological Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Department of Science and Technology, Ministry of Science and Technology, India
  • Indian Council of Medical Research
  • University Grants Commission
Topics
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
oxidative stress, antioxidant status, antidepressants, depression, restraint stress, fluoxetine, imipramine, venlafaxine, superoxide dismutase, catalase, glutathione, lipid peroxidation, protein carbonylation, neuroprotection, stress management
MeSH terms
Venlafaxine Hydrochloride, Animals, Antidepressive Agents, Antidepressive Agents, Tricyclic, Antioxidants, Body Weight, Cyclohexanols, Depressive Disorder, Food Preferences, Imipramine, Restraint, Physical, Stress, Psychological, Swimming, Taste, Lipid Peroxidation, Fluvoxamine, Antidepressive Agents, Second-Generation, Protein Carbonylation, Rats

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