Effect of acute and chronic ethanol intoxication on hepatic regeneration.
We studied the effects of acute and chronic ethanol feeding on hepatic regeneration in rats following partial hepatectomy and toxic liver injury produced by D-galactosamine. Ethanol, when administered as a single dose (6 gm/kg), inhibited 3H-thymidine incorporation into hepatic DNA; this effect depended in part on the time of ethanol feeding following partial hepatectomy. Multiple ethanol feedings produced an even greater inhibition, which persisted for at least 48 hr after partial hepatectomy. Rats chronically fed ethanol for 30 days also failed to achieve a hepatic proliferative response to either partial hepatectomy or D-galactosamine induced hepatitis comparable to isocaloric pair-fed controls. These investigations suggest that there may be a certain metabolic state in the hepatocyte cell cycle which is most susceptible to the action(s) of ethanol; inhibition of liver regeneration by acute or chronic ethanol consumption may result in delayed recovery from prior or coincident liver injury.
D000435:Alcoholic Intoxication / Q000503:physiopathology*; D000437:Alcoholism / Q000503:physiopathology*; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D056486:Chemical and Drug Induced Liver Injury / Q000503:physiopathology; D004032:Diet; D000431:Ethanol / Q000494:pharmacology; D005260:Female; D005688:Galactosamine / Q000633:toxicity; D006801:Humans; D008115:Liver Regeneration; D051381:Rats; D013936:Thymidine / Q000378:metabolism
D000431:Ethanol; D005688:Galactosamine; D001219:Aspartate Aminotransferases; D013936:Thymidine