Rat liver storage iron and plasma ferritin during D-galactosamine-HCl-induced hepatitis.
1. D-Galactosamine-HCl induces toxic hepatitis in the rat and was used as a model to study some aspects of iron metabolism during liver cell damage. Some changes in iron metabolism were similar to those encountered in human acute viral hepatitis. 2. During the first 3 days of liver cell damage induced by galactosamine, liver depot iron and especially ferritin iron decreased by approximately 20%. Plasma ferritin rose, with a peak mean value which was approximately 20 times the concentration measured in normal rats. 3. During the acute phase, plasma ferritin did not accurately reflect the change in the level of liver depot iron. 4. During and after the acute phase, liver depot iron increased after an initial decrease. The non-ferritin depot iron fraction was elevated approximately 75% compared with the value in normal rats. This increase in non-ferritin iron was probably caused by increased erythrocyte catabolism in the liver and recapture followed by catabolism of liver ferritin that had leaked into the blood.
D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000378:metabolism*; D005293:Ferritins / Q000097:blood*; D005688:Galactosamine; D006851:Hydrochloric Acid; D007501:Iron / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008297:Male; D051381:Rats
D005688:Galactosamine; D005293:Ferritins; D007501:Iron; D006851:Hydrochloric Acid