The role of acetaldehyde in the deleterious effects triggered by binge ethanol exposure on synaptic mitochondrial bioenergetics.

KARADAYIAN, A.G.; CZERNICZYNIEC, A.; CARRERE, L.; GUERRA, J.I.; LORES ARNAIZ, S.

Mar del Plata

Congreso; LXVII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2022

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 (BAC) approaches zero. We demonstrated that AH induced strong oxidative stress, mitochondrial dysfunction and alterations in nitric oxide (NO) metabolism in brain cortex synapses, together with the induction of apoptosis signaling pathways. The aim of the present work was to assess the role of acetaldehyde in AH deleterious effects on mitochondrial function at brain cortex synapses using 4-methylpyrazole (4MP), an inhibitor of alcohol dehydrogenase (ADH). Swiss male mice were divided in four different experimental conditions which received i.p. injections of saline (control group), 4MP (10 mg/kg), ethanol (3.8 g/kg, AH group), and 4MP-ethanol. Animals were sacrificed 6h afterwards (BAC=0). Determinations were conducted in brain cortex synaptosomes. The reduction of acetaldehyde levels significantly restored respiration driving ATP synthesis and coupling efficiency by a 5-fold enhancement as compared with AH group (p