Free radical production and antioxidant status in brain cortex non-synaptic mitochondria and synaptosomes at alcohol hangover onset

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

FREE RADICAL BIOLOGY AND MEDICINE

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2017 vol. 108 p. 692 - 703

0891-5849

Alcohol hangover (AH) is the pathophysiological state after abinge-like drinking. We have previously demonstrated that AH inducedbioenergetics impairments in a total fresh mitochondrial fraction inbrain cortex and cerebellum. The aim of this work was to determine freeradical production and antioxidant systems in non-synaptic mitochondriaand synaptosomes in control and hangover animals. Superoxide productionwas not modified in non-synaptic mitochondria while a 17.5% increase wasobserved in synaptosomes. A similar response was observed for cardiolipincontent as no changes were evidenced in non-synaptic mitochondria while a55% decrease in cardiolipin content was found in synaptosomes. Hydrogenperoxide production was 3-fold increased in non-synaptic mitochondria and4-fold increased in synaptosomes. In the presence of deprenyl,synaptosomal H2O2 production was 67% decreased in the AH conditioncompared with the same condition without deprenyl. Hydrogen peroxidegeneration was not affected by deprenyl addition in non-synapticmitochondria from AH mice. MAO activity was 57% increased in non-synapticmitochondria and 3-fold increased in synaptosomes. Catalase activity was40% and 50% decreased in non-synaptic mitochondria and synaptosomes,respectively. Superoxide dismutase was 60% decreased in non-synapticmitochondria and 80% increased in synaptosomal fractions. On the otherhand, GSH content was 43% and 17% decreased in synaptosomes and cytosol.GSH-related enzymes were mostly affected in synaptosomes fractions by AHcondition. Acetylcholinesterase activity in synaptosomes was 11%increased due to AH. The present work reveals that AH provokes animbalance in the cellular redox homeostasis mainly affecting mitochondriapresent in synaptic terminals.