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dc.contributor.author | Karadayian, Analía G. | |
dc.contributor.author | Carrere, Lautaro | |
dc.contributor.author | Czerniczyniec, Analia | |
dc.contributor.author | Lores-Arnaiz, Silvia | |
dc.date.accessioned | 2025-10-21T16:57:07Z | |
dc.date.available | 2025-10-21T16:57:07Z | |
dc.date.issued | 2025-09-17 | |
dc.identifier.citation | Karadayian AG, Carrere L, Czerniczyniec A, Lores-Arnaiz S. Molecular mechanism underlying alcohol’s residual effects: The role of acetaldehyde in mitochondrial dysfunction at synapses in mouse brain cortex. Alcohol. 17 de septiembre de 2025;129:79-91. | es_ES |
dc.identifier.uri | https://doi.org/10.1016/j.alcohol.2025.09.004 | |
dc.identifier.uri | https://repositorio.fleni.org.ar/xmlui/handle/123456789/1419 | |
dc.description.abstract | Alcohol residual effects impose significant physiological and cognitive burdens due to acute ethanol exposure; however, its underlying mechanisms remain poorly understood. This study investigates the role of acetaldehyde, the main ethanol metabolite, in driving mitochondrial dysfunction and synaptic impairment during hangover onset. Using a mice model, we evaluated the effects of ethanol (3.8 g/kg) and the alcohol dehydrogenase inhibitor 4-methylpyrazole (4-MP) on brain cortex synaptosomes. Ethanol exposure significantly elevated serum acetaldehyde compared with control (p < 0.05), and induced mitochondrial dysfunction, as evidenced by impaired respiration (30 % decrease in basal O2 uptake vs. control), mitochondrial membrane depolarization and reduced ATP production (50 % decrease vs. control). These effects were mitigated by pre-treatment with 4-MP, which normalized acetaldehyde levels and partially restored mitochondrial function. Notably, ethanol downregulated synaptic proteins (nNOS, GluN2B, PSD-95; p < 0.05), but 4-MP failed to prevent this reduction, suggesting that acetaldehyde would not be involved in synaptic proteins alterations. Further, ethanol disrupted calcium homeostasis and nitric oxide (NO) content. Interestingly, 4-MP alone also reduced calcium uptake and NO content (p < 0.05), indicating potential off-target effects on neuronal signaling. While the reduction in acetaldehyde levels preserved mitochondrial integrity, its inability to rescue synaptic protein loss highlights the complexity of hangover pathology, involving both acetaldehyde-dependent and -independent mechanisms. Our findings underscore acetaldehyde's pivotal role in hangover-associated mitochondrial dysfunction but reveal divergent pathways in synaptic impairment. These insights advance the search for targeted hangover therapies by delineating acetaldehyde-dependent toxicity. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Elsevier | es_ES |
dc.subject | Alcoholism | es_ES |
dc.subject | Alcoholismo | es_ES |
dc.subject | Mitochondrial Diseases | es_ES |
dc.subject | Enfermedades Mitocondriales | es_ES |
dc.subject | Acetaldehyde | es_ES |
dc.subject | Acetaldehído | es_ES |
dc.subject | Fomepizole | es_ES |
dc.subject | Fomepizol | es_ES |
dc.title | Molecular mechanism underlying alcohol's residual effects: The role of acetaldehyde in mitochondrial dysfunction at synapses in mouse brain cortex | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.description.fil | Fil: Czerniczyniec, Analia. Fleni. Instituto de Neurociencias FLENI-CONICET. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. | |
dc.relation.ispartofVOLUME | 129 | |
dc.relation.ispartofPAGINATION | 79-91 | |
dc.relation.ispartofCOUNTRY | Estados Unidos | |
dc.relation.ispartofCITY | Nueva York | |
dc.relation.ispartofTITLE | Alcohol | |
dc.relation.ispartofISSN | 1873-6823 | |
dc.type.snrd | info:ar-repo/semantics/artículo | es_ES |