Abstract
Acute ethanol administration significantly increased the concentration of adenosine monophosphate (5′-AMP) in the intact freeze-clamped rat liver regardless of the ethanol dose administered. The increase was abolished by the alcohol dehydrogenase inhibitor 4-methylpyrazole, but was also seen after direct infusion of acetaldehyde into the portal vein. Administration of acetate to give hepatic levels similar to those seen during ethanol oxidation failed, however, to cause an increase in AMP. After ethanol administration there was a highly significant positive correlation between individual AMP levels and 3-OH-butyrate/acetoacetate ratios. The results suggest that the increase in liver AMP reflects activation of ethanol-derived acetate by acetothiokinase in the mitochondrial matrix. Ethanol, but not acetate inhibits the citric acid cycle, as reflected by the shift in the mitochondrial redox state. This could inhibit production of GTP needed for AMP phosphorylation by GTP-AMP phosphotransferase, thus explaining the accumulation
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