Acute or repeated cocaine administration generates reactive oxygen species and induces antioxidant enzyme activity in dopaminergic rat brain structures

Diétrich, Jacques; Mangeol, Aude; Revel, Marie‐Odile; Burgun, Claude; Aunis, Dominique; Zwiller, Jean

doi:10.1016/j.neuropharm.2005.01.018

Cited by 145 publications

(134 citation statements)

References 32 publications

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“…However, morphological features of apoptosis were not evident upon in vivo (Dietrich et al, 2005) or in vitro (Oliveira et al, 2002;Cunha-Oliveira et al, 2006a) exposure to cocaine, except in one study from Nassogne et al (1997). Cell death induced by cocaine in human neuronal progenitor cells, involving cytochrome c release, seems to be preceded by oxidative stress (Poon et al, 2007).…”

Section: Cocaine and Apoptosis Cocaine Neurotoxicity Hasmentioning

confidence: 91%

“…The occurrence of oxidative stress in neurons, upon exposure to cocaine has been much less studied, when compared to amphetamine and amphetamine derivatives. Cocaine exposure has been reported to increase H 2 O 2 in the prefrontal cortex and in the striatum of rats (Dietrich et al, 2005). Cocaine exposure was also shown to induce a decrease in catalase activity (Macedo et al, 2005), as well as an increase in SOD and GPx activities (Dietrich et al, 2005) in the cortex and in the striatum of animals.…”

Section: 4mentioning

confidence: 95%

“…Cocaine exposure has been reported to increase H 2 O 2 in the prefrontal cortex and in the striatum of rats (Dietrich et al, 2005). Cocaine exposure was also shown to induce a decrease in catalase activity (Macedo et al, 2005), as well as an increase in SOD and GPx activities (Dietrich et al, 2005) in the cortex and in the striatum of animals. The levels of antioxidants such as GSH or reduced vitamin E have been also shown to be decreased upon cocaine exposure (Poon et al, 2007;Lipton et al, 2003).…”

Section: 4mentioning

confidence: 95%

“…Some studies also implicated p53 in the apoptotic process induced by D-amphetamine (Krasnova et al, 2005) and methamphetamine (Imam et al, 2001). Morphological features of apoptosis induced by D-amphetamine were observed upon in vitro (Oliveira et al, 2002;CunhaOliveira et al, 2006a) and in vivo (Dietrich et al, 2005) exposure. Furthermore, TUNEL-positive cells were observed in the striatum of methamphetamine exposed mice (Zhu et al, 2006).…”

mentioning

confidence: 97%

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Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cunha‐Oliveira

Rego

Oliveira

2008

Brain Research Reviews

189

131

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Section: Cocaine and Apoptosis Cocaine Neurotoxicity Hasmentioning

confidence: 91%

Section: 4mentioning

confidence: 95%

Section: 4mentioning

confidence: 95%

mentioning

confidence: 97%

See 2 more Smart Citations

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cunha‐Oliveira

Rego

Oliveira

2008

Brain Research Reviews

189

131

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“…Figure 5a is representative of protein identification in this study. The GFAP identification was validated by sequencing two peptides, ALAAELNQLR [94][95][96][97][98][99][100][101][102][103] and LADVYQAELR, [110][111][112][113][114][115][116][117][118][119] having precursor ion m/z of 1098.6 and 1177.6, respectively (Figure 5b and c). Some of the protein spots that yielded significant DeCyder ratios were not identified with MALDI-ToF-MS, which can be attributed to insufficient amounts of protein.…”

Section: Methodological Considerationsmentioning

confidence: 99%

Cytosolic proteomic alterations in the nucleus accumbens of cocaine overdose victims

2006

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Chronic cocaine use in humans and animal models is known to lead to pronounced alterations in neuronal function in the nucleus accumbens (NAc), a brain region associated with drug reinforcement. Two-dimensional gel electrophoresis was used to compare protein alterations in the NAc between cocaine overdose (COD) victims (n = 10) and controls (n = 10). Following image normalization, spots with significantly differential image intensities (P < 0.05) were identified, excised, trypsin digested and analyzed by matrix-assisted laser desorption ionization-time of flight-time of flight. A total of 1407 spots were found to be present in a minimum of five subjects per group and the intensity of 18 spots was found to be differentially abundant between the groups, leading to positive identification of 15 proteins by peptide mass fingerprinting (PMF). Of an additional 37 protein spots that were constitutively expressed, 32 proteins were positively identified by PMF. Increased proteins in COD included b-tubulin, liprin-a3 and neuronal enolase, whereas decreased proteins included parvalbumin, ATP synthase b-chain and peroxiredoxin 2. The present data provide a preliminary protein profile of COD, suggesting the involvement of novel proteins and pathways in the expression of this complex disease. Additional studies are warranted to further characterize alterations in the differentially regulated proteins. Understanding the coordinated involvement of multiple proteins in cocaine abuse provides insight into the molecular basis of the disease and offers new targets for pharmacotherapeutic intervention for drug abuse-related disorders.

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Total antioxidant capacity is significantly lower in cocaine‐dependent and methamphetamine‐dependent patients relative to normal controls: results from a preliminary study

Walker

Winhusen

Storkson

et al. 2014

Human Psychopharmacology

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Background Oxidative stress can result in damage to the brain and other organs. To protect from oxidative damage, the human body possesses molecular defense systems, based on the activity of antioxidants, and enzymatic defense systems, including the enzymes catalase (CAT), superoxide-dismutase (SOD) and glutathione-peroxidase (GPx). While pre-clinical research has shown that stimulant use is associated with oxidative damage, oxidative stress and the antioxidant defense systems have not been evaluated in clinical samples of stimulant-dependent patients. Objectives This study aimed to investigate the link between stimulant dependence and oxidative stress. Methods Peripheral blood samples from 174 methamphetamine (n=48) and/or cocaine-dependent (n=126) participants as well as 30 normal control participants were analyzed for the enzyme activities of CAT, SOD and GPx in the erythrocytes, and the total antioxidant capacity and the malondialdehyde concentration in the plasma. Results We could show an association of stimulant dependence with a depletion of total antioxidant capacity to 54.6±4.7 %, which correlates with a reduced activity of the SOD to 71.3±0.03 % compared to healthy control participants (100 %). Conclusion Stimulant-dependent patients had significantly lower antioxidant capacity relative to controls, suggesting that they may be at greater risk for oxidative damage to the brain and other organs.

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Acute or repeated cocaine administration generates reactive oxygen species and induces antioxidant enzyme activity in dopaminergic rat brain structures

Cited by 145 publications

References 32 publications

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cytosolic proteomic alterations in the nucleus accumbens of cocaine overdose victims

Total antioxidant capacity is significantly lower in cocaine‐dependent and methamphetamine‐dependent patients relative to normal controls: results from a preliminary study

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