Abstract
The administration of adenosine partially prevented and reverted the ethanol-induced fatty liver. The hepatic α-glycerophosphate concentration and the α-glycerophosphate/dihydroxyacetone phosphate ratio were significantly increased after ethanol administration. The nucleoside decreased with ratio and enhanced the oxidation of ethanol. A strong correlation between the cytoplasmic redox state and the amount of triacylglycerols in the liver was found (8 h after treatments) stressing the paramount importance of the redox state in the pathogenesis of ethanol-induced fatty liver. As previously reported, the nucleoside expanded the adenine nucleotide pool size and the hepatic ATP level. Ethanol potentiated these effects. It is suggested that adenosine ameliorated the ethanol-induced fatty liver through an increased utilization of reducing equivalents by the mitochondria. An interdependence of these effects is proposed and discussed.
Published Version
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