Influence of hypoxia on the hepatotoxic effects of carbon tetrachloride, paracetamol, allyl alcohol, bromobenzene and thioacetamide.
Exposure of rats to a reduced oxygen tension (6% O2, 94% N2) for 6 h increased the serum enzyme and the histological lesions induced by carbon tetrachloride (CCl4). Hypoxia did not enhance the hepatotoxic response to paracetamol, allyl alcohol, bromobenzene or thioacetamide. No correlation was found between the changes in hepatotoxicity induced by hypoxia and those after treatment with ethanol. Hepatic hypoxia therefore was not the pathogenetic mechanism responsible for ethanol-induced enhancement of hepatotoxicity.
D000082:Acetaminophen / Q000633:toxicity; D000498:Allyl Compounds / Q000633:toxicity*; D000818:Animals; D001969:Bromobenzenes / Q000633:toxicity; D002251:Carbon Tetrachloride / Q000633:toxicity*; D000431:Ethanol / Q000633:toxicity*; D006439:Hemodynamics / Q000187:drug effects; D000860:Hypoxia / Q000503:physiopathology*; D008099:Liver / Q000187:drug effects* / Q000473:pathology; D008297:Male; D051381:Rats; D013853:Thioacetamide / Q000633:toxicity
D000498:Allyl Compounds; D001969:Bromobenzenes; D013853:Thioacetamide; D000082:Acetaminophen; D000431:Ethanol; D002251:Carbon Tetrachloride