HEPATIC GLUTATHIONE LEVELS IN D-PENICILLAMINE-FED ETHANOL-DEPENDENT RATS

Google Scholar
  • 1 January 1979
    • journal article
    • research article
    • Vol. 25  (2) , 389-394
Abstract
Ethanol oxidation is accomplished primarily by alcohol dehydrogenase. A microsomal system involving hydrogen peroxide formation operates at elevated ethanol concentrations. Removal of the resultant hydrogen peroxide may depend on the activity of glutathione peroxidase. The effect of chronic ethanol exposure on hepatic glutathione levels was examined. Ethanol exposure resulted in elevations of hepatic reduced and oxidized glutathione. The dietary inclusion of the sulfhydryl amino acid, D-penicillamine, increase hepatic reduced glutathione (GSH) in both ethanol-dependent and control rats. D-penicillamine did not have a differential effect on hepatic GSH when comparing ethanol-dependent and control animals. Following 2 wk exposure, the exclusion of ethanol and/or D-penicillamine from the diet for 24 h resulted in a significant decrease in hepatic GSH.