Apoptosis Due to After-effects of Acute Ethanol Exposure in Brain Cortex: Intrinsic and Extrinsic Signaling Pathways

KARADAYIAN, ANALÍA G.; CZERNICZYNIEC, ANALIA; LORES-ARNAIZ, SILVIA

NEUROSCIENCE

PERGAMON-ELSEVIER SCIENCE LTD

Año: 2024 vol. 544 p. 39 - 49

0306-4522

Alcohol hangover is the combination of negative mental and physical symptoms which can be experiencedafter a single episode of alcohol consumption, starting when blood alcohol concentration approaches zero.We previously demonstrated that hangover provokes mitochondrial dysfunction, oxidative stress, imbalance inantioxidant defenses, and impairment in cellular bioenergetics. Chronic and acute ethanol intake induces neu-roapoptosis but there are no studies which evaluated apoptosis at alcohol hangover. The aim of the present workwas to study alcohol residual effects on intrinsic and extrinsic apoptotic signaling pathways in mice brain cortex.Male Swiss mice received i.p. injection of ethanol (3.8 g/kg) or saline. Six hours after injection, at alcohol hangoveronset, mitochondria and tissue lysates were obtained from brain cortex. Results indicated that during alcoholhangover a loss of granularity of mitochondria and a strong increment in mitochondrial permeability wereobserved, indicating the occurrence of swelling. Alcohol-treated mice showed a significant 35% increase inBax/Bcl-2 ratio and a 5-fold increase in the ratio level of cytochrome c between mitochondria and cytosol. Caspase3, 8 and 9 protein expressions were 32%, 33% and 20% respectively enhanced and the activity of caspase3 and 6 was 30% and 20% increased also due to the hangover condition. Moreover, 38% and 32% increments werefound in PARP1 and p53 protein expression respectively and on the contrary, SIRT-1 was almost 50% lower thancontrols due to the hangover condition. The present work demonstrates that alcohol after-effects could result inthe activation of mitochondrial and non-mitochondrial apoptosis pathways. 2024 IBRO. Published by Elsevier Inc. Allrights reserved.