Unraveling molecular mechanisms involved in after-effects of acute ethanol exposure in brain cortex. The dual contribution of mitochondrial dysfunction and oxidative stress in triggering apoptosis.

KARADAYIAN, A.G., ; CZERNICZYNIEC, A.; LORES ARNAIZ, S.

Buenos Aires

Congreso; V International Congress in Translational Medicine, Buenos aires; 2021

Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires

The abuse of alcohol consumption is a type of alcohol-related disorder causing several serious consequences to health. The most common consumption pattern, particularly among adolescents and young adults, is the so-called ?binge drinking? whose direct consequence is defined as alcohol hangover (AH). AH is defined as a combination of mental and physical symptoms experienced the day after a single episode of heavy drinking, starting when blood alcohol concentration (BAC) approaches zero. Recently, we demonstrated that alcohol after-effects include strong oxidative stress, mitochondrial dysfunction and alterations in nitric oxide (NO) metabolism through the impairment of NMDAR/PSD-95/nNOS pathway at brain cortex synapses. The aim of the present work was to study apoptosis signaling in AH in association with changes in NO metabolism and mitochondrial bioenergetics. Swiss male mice received an i.p. injection of ethanol (3.8 g/kg body weight, AH group) or saline (control group) and were sacrificed 6 h afterwards (BAC=0). Determinations were conducted in three different samples: brain cortex synaptosomes, crude mitochondria and brain lysates. In synaptosomal membranes from AH mice, glutamate-induced calcium influx determined by flow cytometry was significantly decreased (p