[Toxicity of ammonium acetate in rats with acute and subacute galactosamine-induced hepatitis (author's transl)].
Ammonia toxicity and the protective effect of arginine thereon were investigated in rats after single and repeated doses of galactosamine. Urea cycle enzymes and ornithine-oxo-acid transaminase activities were measured in rat liver homogenates. Ammonium acetate proved to be less toxic in rats treated with single or repeated doses of galactosamine than in untreated animals. Urea cycle enzyme activities of galactosamine-treated rats were clearly lowered. The protective effect of arginine against lethal ammonia intoxication was found in animals that had been treated with galactosamine as well as in untreated rats. Since the toxicity of ammonium acetate is lower in rats with galactosamine hepatitis, in which the activities of the liver urea cycle enzymes are reduced, it seems likely that ammonia detoxication in galactosamine-poisoned rat liver partly bypasses the urea cycle.
D000085:Acetates; D000818:Animals; D001120:Arginine / Q000494:pharmacology; D056486:Chemical and Drug Induced Liver Injury; D005260:Female; D005688:Galactosamine; D006505:Hepatitis / Q000503:physiopathology*; D000644:Quaternary Ammonium Compounds / Q000633:toxicity*; D051381:Rats; D014508:Urea / Q000378:metabolism
D000085:Acetates; D000644:Quaternary Ammonium Compounds; D005688:Galactosamine; D014508:Urea; D001120:Arginine; C018824:ammonium acetate
Toxizität von Ammoniumacetat bei Ratten mit akuter und subakuter Galactosamin-Hepatitis.