Oxidative stress induced by acute alcohol exposure in mouse brain cortex non-synaptic mitochondria and synaptosomes

KARADAYIAN AG; CZERNICZYNIEC A; MALANGA G.; LOMBARDI P, BUSTAMANTE J, LORES ARNAIZ S. ; BUSTAMANTE J; LORES ARNAIZ S

CABA

Congreso; 2nd Federation of Latinamerican Neuroscience Societies (FALAN) Congress; 2016

Binge alcohol drinking causes a number of serious consequences to health. We previously demonstrated that alcohol hangover (AH) induced oxidative stress in brain cortex and cerebellum, evidenced in total mitochondrial fractions. The aim of this work was to study the production of active oxygen species and antioxidant enzymes activities at the beginning of AH in brain cortex non-synaptic mitochondria (NSm) and synaptosomes (S). Swiss male mice were treated with a single i.p. injection of saline (control group) or ethanol (3.8 g/kg; AH group). Biochemical assays were performed 6 h post-treatment when blood alcohol concentration was close to zero (AH start). Results showed a 17.5% increase in superoxide anion production together with a 50% decrease in cardiolipin content in S fraction. In contrast, superoxide anion and cardiolipin content was unaltered in NSm. Hydrogen peroxide production was 3-fold increased in NSm and 4-times increased in S fractions. Monoamine oxidase activity was 57% increased in NSm and 3-fold increased in S fractions. Catalase activity was 40% and 50% decreased in NSm and S, respectively. Superoxide dismutase was 60% decreased in NSm and 80% increased in S fractions. On the other hand, GSH content was 94% decreased together with significant decreases in GSH-related enzymes in S fractions. Based on these findings, it is postulated that AH induce an imbalance in the cellular redox homeostasis mainly affecting mitochondria present in synaptic terminals.