Nitric oxide and apoptosis due to afterNitric oxide and apoptosis due to after-effects of acute ethanol exposure in brain cortex-effects of acute ethanol exposure in brain cortex

ANALIA G. KARADAYIAN; SILVIA LORES ARNAIZ; JUANITA BUSTAMANTE; ANALIA CZERNICZYNIEC

Mar del Plata

Congreso; LXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2019

Sociedad Argentina de Investigación Clínica

Alcohol hangover (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 approaches to zero. We previously evidenced bioenergetics alterations and oxidative stress in brain cortex synaptosomes from AH mice. The aim of the present work was to study the after-effects of acute ethanol administration on nitric oxide (NO) metabolism, mitochondrial calcium uptake and induction of apoptosis. 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. Synaptosomal NOS activity and total NO levels were determined, as well as the expression of nNOS, iNOS, PSD-95 and the NR2B-subunit of NMDA receptor. Mitochondrial calcium uptake, permeability transition (MPT) and the expression of apoptotic markers were analyzed in mitochondrial fractions. Results showed a 35-37% decrease in NOS activity and total NO content in AH mice (p