Enhanced hepatotoxicity of carbon tetrachloride following sodium nitrite pretreatment.
The administration of sodium nitrite (60 mg/kg, s.c.) 30 min prior to carbon tetrachloride intoxication (2 ml/kg, p.o.) significantly enhanced the rise in serum glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and isocitrate dehydrogenase. Sodium nitrite pretreatment also enhanced the carbon tetrachloride-induced decrease in hepatic microsomal glucose-6-phosphatase activity. Microsomal diene conjugation absorption indicative of microsomal lipid peroxidation was observed following carbon tetrachloride intoxication, but was not altered by sodium nitrite pretreatment. The data indicate a potentially toxic interaction between sodium nitrite-induced methemoglobinemia and carbon tetrachloride-induced hepatic injury.
D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000503:physiopathology*; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology*; D004357:Drug Synergism; D000860:Hypoxia / Q000503:physiopathology; D050356:Lipid Metabolism; D008297:Male; D008708:Methemoglobinemia / Q000139:chemically induced; D009573:Nitrites / Q000494:pharmacology*; D010545:Peroxides / Q000378:metabolism; D051381:Rats; D012977:Sodium Nitrite / Q000494:pharmacology*; D013997:Time Factors
D009573:Nitrites; D010545:Peroxides; D012977:Sodium Nitrite