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Acute or repeated cocaine administration generates reactive oxygen species and induces antioxidant enzyme activity in dopaminergic rat brain structures
Abstract
Either a single (acute) or repeated daily (chronic) injections (1 injection/day) of 20 mg/kg cocaine for 10 days to rats was found to increase reactive oxygen species production in two dopaminergic brain structures, the frontal cortex and the striatum. We found that the mitochondrial genome was down-regulated after acute cocaine injection. Hydroperoxide and lipid peroxide generation was correlated with an increase in mitochondrial hydrogen peroxide generation and with a reduced functioning of mitochondrial complex I in response to cocaine. As judged from the measurement of caspase-3 activity and TUNEL labeling, neither acute nor chronic cocaine treatment has been found to induce apoptosis in any of the structures examined. This differs dramatically from what has been described for methamphetamine. Cocaine-induced radical formation was accompanied by the induction of the antioxidant enzymes superoxide dismutase and glutathione peroxidase, after both acute and chronic cocaine treatment. In addition, proteasome chymotrypsin-like activity was enhanced following a single cocaine injection in both cortex and striatum. It is proposed that the compensatory mechanisms to oxidative stress occurring in response to cocaine were effective in scavenging reactive oxygen species and in preventing subsequent cellular damage, thus explaining why no significant cell death was found in these brain structures.
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“Cocaine produces oxidative stress in neurons (Dietrich et al., 2005;Numa et al., 2008;Jang et al., 2014;Sordi et al., 2014).”
From Casting a Wide Net: Role of Perineuronal Nets in Neural Plasticity (2016) · cites this paper as Dietrich et al., 2005
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Oxidative stress in psychiatric disorders: evidence base and therapeutic implications
Ng, F., Berk, M., Dean, O., & Bush, A. I. (2008) · The International Journal of Neuropsychopharmacology · doi:10.1017/s1461145707008401 · Cited by 1,069
“, 2005), cocaine (Dietrich et al., 2005) and amphetamines (Frey et al.”
BackgroundCasting a Wide Net: Role of Perineuronal Nets in Neural Plasticity
Sorg, B. A., Berretta, S., Blacktop, J. M., Fawcett, J. W., Kitagawa, H., Kwok, J. C. F., & Miquel, M. (2016) · The Journal of Neuroscience · doi:10.1523/jneurosci.2351-16.2016 · Cited by 454
“Cocaine produces oxidative stress in neurons (Dietrich et al., 2005; Numa et al., 2008; Sordi et al., 2014; Jang et al., 2015).”
Nuclear Factor κB Signaling Regulates Neuronal Morphology and Cocaine Reward
Russo, S. J., Wilkinson, M. B., Mazei‐Robison, M. S., Dietz, D., Maze, I. S., Krishnan, V., Renthal, W. R., Graham, A., Birnbaum, S. G., Green, T. A., et al. (2009) · Journal of Neuroscience · doi:10.1523/jneurosci.6173-08.2009 · Cited by 248
“In contrast to methamphetamine, cocaine, at least at the dosing schedules used here, does not induce cell death or frank injury in the CNS (Dietrich et al., 2005), although it has been shown to alter cell morphology in the NAc and certain other reward-related brain structures (Li et al., 2004;…”
BackgroundCellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs
Cunha‐Oliveira, T., Rego, A. C., & Oliveira, C. R. (2008) · Brain Research Reviews · doi:10.1016/j.brainresrev.2008.03.002 · Cited by 243
“Cocaine seems to be less toxic than amphetamine, and in most studies apoptotic neuronswere not observed upon exposure to cocaine (Dietrich et al., 2005; Cunha-Oliveira et al., 2006a; Oliveira et al., 2002).”
BackgroundInfluentialNelson, S. K., Bose, S. K., Grunwald, G. K., Myhill, P., & McCord, J. M. (2006) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2005.08.043 · Cited by 215
Metadata
- Authors
- Dietrich, J.-B., Mangeol, A., Revel, M.-O., Burgun, C., Aunis, D., & Zwiller, J.
- Affiliations
- Inserm (FR)
- Corresponding author
- Dietrich, Jean-Bernard
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2005-06
- Volume
- 48
- Issue
- 7
- Pages
- 965-974
- ISSN
- 0028-3908 (ISSN-L)
- OpenAlex
- W2061764945
- Cited by
- 168
- References
- 34
- Citations by year
- 2026: 8 · 2025: 5 · 2024: 4 · 2023: 5 · 2022: 7 · 2021: 13 · 2020: 5 · 2019: 11 · 2018: 13 · 2017: 7 · 2016: 9 · 2015: 9 · 2014: 16 · 2013: 11 · 2012: 8
- FWCI
- 2.16
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- cocaine, reactive oxygen species, oxidative stress, antioxidant enzymes, superoxide dismutase, glutathione peroxidase, dopaminergic neurons, frontal cortex, striatum, mitochondrial hydrogen peroxide, mitochondrial complex I, lipid peroxidation, caspase-3, apoptosis, methamphetamine
- MeSH terms
- Animals, Antioxidants, Brain, Cocaine, Dopamine, Enzyme Induction, Glutathione Peroxidase, Male, Superoxide Dismutase, Rats, Wistar, Reactive Oxygen Species, Rats
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