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Effect of Chronic Ethanol Ingestion on Liver Enzyme Changes Induced by Thiamine, Riboflavin, Pyridoxine, or Choline Deficiency^1,2,

Department of Pathology, San Francisco General Hospital, University of California School of Medicine, San Francisco, California

The effect of ethanol on riboflavin, pyridoxine, thiamine, and choline deficiencies was studied by measuring changes in rat liver dehydrogenases and by histologic assessment of fatty change in the liver. Ethanol ingestion lessened the changes induced by riboflavin deficiency. A diminution of succinic dehydrogenase (SD) activity was induced by riboflavin deficiency; however, in ethanol-fed rats this activity was significantly less diminished, and the fatty liver observed in the riboflavin-deficient animals was prevented. In contrast, the combination of ethanol ingestion and pyridoxine deficiency caused a reduction in ß-hydroxybutyric dehydrogenase (HBD) activity and caused a fatty liver, whereas pyridoxine deficiency alone or ethanol feeding alone did not. Thiamine deficiency decreased the activities of HBD and lactic (LD) dehydrogenases; these depressed levels were unaffected by ethanol ingestion. The combination of choline deficiency and ethanol ingestion decreased the activities of HBD and nicotinamide-adenine dinucleotide phosphate (NADPH) dehydrogenases; however, the activity of NADPH dehydrogenase was also reduced by either choline deficiency or ethanol alone. The data suggest that ethanol ingestion is more deleterious to pyridoxine-deficient rats than to controls.

² Presented in part at the 49th Annual Meeting of the Federation of American Societies for Experimental Biology, 1965, Atlantic City, New Jersey (Federation Proc., 24: 557, 1965 (abstract)).

Manuscript received 18 October 1965.