Effects of vitamin E on D-galactosamine-induced or carbon tetrachloride-induced hepatotoxicity.
Experimental liver disorders were induced by the use of carbon tetrachloride or D-galactosamine hydrochloride in rats maintained on a vitamin E deficient diet and in rats fed a diet supplemented with vitamin E, and the protective effect of vitamin E on the liver was determined. After exposure to carbon tetrachloride or D-galactosamine hydrochloride the serum levels of transaminases, lysosomal enzyme beta-glucuronidase, and acid phosphatase were elevated, and thiobarbituric acid reactive substances in serum and liver homogenate were also increased. The changes were conspicuous in the vitamin E deficient rats, but were only slight in rats fed a diet supplemented with vitamin E. The results of this study suggest that vitamin E has a protective effect on liver disorders by inhibiting lysosomal enzyme liberation and lipid peroxidation.
D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000150:complications; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy*; D005260:Female; D005688:Galactosamine; D008099:Liver / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D008247:Lysosomes / Q000201:enzymology; D051381:Rats; D011919:Rats, Inbred Strains; D013858:Thiobarbiturates / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology / Q000627:therapeutic use*
D013858:Thiobarbiturates; D014810:Vitamin E; D005688:Galactosamine; C029684:thiobarbituric acid