Producción CyT
Congreso
Autoría
Karadayian, A.G.
;
Czerniczyniec A.
;
LORES ARNAIZ, SILVIA
Fecha
2021
Editorial y Lugar de Edición
Fundación Revista Medicina
ISSN
1669-9106
Resumen
Información suministrada por el agente en
SIGEVA
Binge-drinking is the most common alcohol-related disorder whose direct consequence is known as alcohol hangover (AH). This one 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 through the impairment of NMDAR/PSD-95/nNOS pathway i...
Binge-drinking is the most common alcohol-related disorder whose direct consequence is known as alcohol hangover (AH). This one 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 through the impairment of NMDAR/PSD-95/nNOS pathway in brain cortex synapses.The aim of the present work was to study apoptotic signaling pathways in brain cortex at the onset of AH. Swiss male 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 (BAC=0). Determinations were conducted in mitochondria and lysates from braincortex. Impairment of calcium handling and MPT induction were observed in AH mitochondria (p<0.05) together with a 21% increase and 18% decrease in Bax and Bcl-2 protein expression (p<0.05) respectively. Moreover, a 4-fold decrease in cytochrome c mitochondria/cytosol ratio was found due to AH (p<0.01). In addition, citrate synthase, a mitochondrial enzyme marker, was 40% decreased in AH mitochondria (p<0.05). Interestingly, AIF protein expression was unchanged by AH. Caspase 3 and 9 activity and expression were increased by approximately 30% and 18-19% respectively (p<0.05) in brain cortex lysates from AH. In addition, although non-significant, p53 was found 14% increased in AH brain cortex (p=0.057). Lastly, SIRT-1, a histone deacetylase which promotes mitochondrial biogenesis was63% decreased (p<0.01).In conclusion, alcohol after-effects could result in the activation of intrinsic apoptotic pathways due to mitochondrial dysfunction and oxidative stress. Also, non-mitochondrial apoptotic processes can be triggered during AH due to the blockage of calcium entry at synapses after disruption of NMDAR/PSD-95/nNOS pathway.
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Palabras Clave
MITOCHONDRIAETHANOL HANGOVERAPOPTOSIS