Impairment in mitochondrial function and free radical production in brain cortex and cerebellum during ethanol hangover

KARADAYIAN ANALÍA GRACIELA; CZERNICZYNIEC ANALIA; BUSTAMANTE JUANITA; LORES-ARNAIZ SILVIA

Buenos Aires

Congreso; VIII Meeting of the Society for Free Radical Biology and Medicine - South American Group; 2013

Society for Free Radical Biology and Medicine - South American Goup

Alcohol hangover is a temporary state described as the unpleasant next-day effects after a binge-like drinking. Acute ethanol administration induces reactive oxygen species production associated to mitochondrial dysfunction. Our aim was to evaluate mitochondrial function and free radical production at hangover onset. Male Swiss mice were injected i.p. either with saline (control group) or with ethanol (3.8 g/kg BW; hangover group) and sacrificed after 6 hours, when blood alcohol levels were zero (hangover onset). A significant decrease in the respiratory control rate was observed in brain cortex and cerebellum mitochondria from hangover mice. Specifically, hangover group exhibited a significant decrease in malate-glutamate and succinate dependent state 3 oxygen consumption in brain cortex, while in cerebellum a marked increase in state 4 respiratory rate was observed. Hydrogen peroxide production was 90% increased in brain cortex and cerebellum in hangover mice. Mitochondrial complex I, II and IV activities were significantly decreased by the hangover condition in brain cortex. Complex I-IIII was 38% decreased in cerebellum from hangover mice. Mitochondrial transmembrane potential results indicated that hangover mice presented 17% depolarization in brain cortex. Our findings suggest that hangover induced mitochondrial dysfunction and increased oxygen free radical production in brain cortex and cerebellum.