Liver and kidney damage induced by N-hydroxyparacetamol.
1. Liver and kidney glutathione are depleted in rats and mice following administration of N-hydroxyparacetamol. 2. Centrilobular hepatic necrosis and necrosis of renal proximal convoluted tubules were also  found, the liver lesion predominantly in mice and the renal lesion predominantly in rats. Glutathione depletion was not responsible for this species difference. 3. These results indicate that N-hydroxyparacetamol is the metabolic precursor of the reactive toxic intermediate of paracetamol. They are also relevant to the pathogenesis of the renal damage associated with long term abuse of phenacetin containing compound analgesics.
D000082:Acetaminophen / Q000031:analogs & derivatives* / Q000032:analysis / Q000494:pharmacology; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology* / Q000473:pathology; D004355:Drug Stability; D005978:Glutathione / Q000378:metabolism; D006900:Hydroxylation; D007668:Kidney / Q000473:pathology; D007674:Kidney Diseases / Q000139:chemically induced* / Q000473:pathology; D008099:Liver / Q000473:pathology; D008297:Male; D051381:Rats
D000082:Acetaminophen; D005978:Glutathione