Acute ethanol exposure alters hepatic glutathione metabolism in riboflavin deficiency.
Since acute ethanol consumption and riboflavin deficiency each induces oxidative stress within tissues, we examined whether their combined effects compromise the major antioxidative system in liver, namely, reduced glutathione (GSH) metabolism. Four hours before sacrifice, half the riboflavin-deficient (RD) and riboflavin-sufficient (RS) rats were treated with ethanol (3 g/kg). Livers were excised and analyzed for GSH and enzymes that control its metabolism. In RD rats, GSH increased while glucose-6-phosphate dehydrogenase (G6PD) activity decreased. Ethanol had no effect on these measurements in RS rats. In RD rats, ethanol administration decreased GSH along with the activities of GSH peroxidase, glutathione reductase, and G6PD. These data suggest that riboflavin deficiency alone does not compromise hepatic GSH metabolism. By contrast, ethanol consumption together with riboflavin deficiency depletes hepatic GSH, blunts enzyme activities controlling GSH metabolism and may enhance alcohol-induced liver injury.[1]References
- Acute ethanol exposure alters hepatic glutathione metabolism in riboflavin deficiency. Dutta, P., Seirafi, J., Halpin, D., Pinto, J., Rivlin, R. Alcohol (1995) [Pubmed]
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