METABOLIC CONSEQUENCES OF ETHANOL OXIDATION IN BRAINS FROM MICE CHRONICALLY FED ETHANOL

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Abstract
Abstract— Effects of the acute and chronic administration of ethanol have been investigated in mouse brain on the redox‐state, citric acid cycle function, levels of adenine nucleotides and other metabolites. Cerebral oxidation of ethanol, activity of alcohol dehydrogenase and the permeability of brain and liver mitochondrial preparations after chronic ethanol administration have been also investigated. Acute or chronic administration of ethanol resulted in a small but significant increase in the reduced components of certain dehydrogenase‐linked substrate pairs in brain. Pyrazole, an inhibitor of alcohol dehydrogenase, prevented the ethanol‐induced changes in brain. 14CO2 production from several substrates was inhibited in brains from chronically ethanol‐fed animals. Addition of pyrazole, however, prevented the ethanol‐mediated inhibition of 14CO2 production. Chronic administration of ethanol resulted in decreased levels of ATP and creatine phosphate in the brain, and increased contents of ADP and AMP. The cerebral activities of alcohol dehydrogenase and succinic dehydrogenase, oxidation of ethanol, mitochondrial oxidation of a‐glycerophosphate, and levels of NADH remained unaffected by the chronic administration of ethanol. In contrast to liver, where chronic administration of ethanol increased the contribution of 'substrate shuttles’resulting in increased oxidation of ethanol; in brain, the contribution of these 'shuttles’remained unaffected.