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ECB-ART-48781
Toxicol Rep 2019 Nov 09;6:1223-1229. doi: 10.1016/j.toxrep.2019.11.001.
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Anhydroecgonine methyl ester (AEME), a cocaine pyrolysis product, impairs glutathione-related enzymes response and increases lipid peroxidation in the hippocampal cell culture.

Garcia RCT , Torres LL , Dati LMM , Loureiro APM , Afeche SC , Sandoval MRL , Marcourakis T .


Abstract
Crack cocaine smokers inhale, alongside with cocaine, its pyrolysis product, anhydroecgonine methyl ester (AEME). We have previously described AEME neurotoxic effect and its additive effect when co-incubated with cocaine. Our aim was to evaluate, the effect of AEME, cocaine and AEME-cocaine combination on glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) activities after 3 and 6 h of exposure, periods previous to neuronal death. Lipid peroxidation was evaluated through malonaldehyde (MDA) levels at 3, 6, 24 and 48 h of exposure. All treated groups reduced neuronal viability after 24 h of exposure. AEME and cocaine decreased GPx, GR and GST activities after 3 and 6 h, with an increase in MDA levels after 48 h. AEME-cocaine combination decreased the enzymes activities after 3 and 6 h, showing an additive effect in MDA levels after 48 h. These data show that the glutathione-related enzymes imbalance caused by AEME, cocaine or AEME-cocaine combination exposure preceded neuronal death and lipid peroxidation. Moreover, the additive effect on lipid peroxidation observed with AEME-cocaine exposure after 48 h, suggest a higher neurotoxic effect after crack cocaine use when compared to cocaine alone.

PubMed ID: 31768333
PMC ID: PMC6872858
Article link: Toxicol Rep


Genes referenced: gsr LOC115919910 LOC594349 LOC752853


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References [+] :
Bashkatova, Nitric oxide and oxidative stress in the brain of rats exposed in utero to cocaine. 2006, Pubmed