Enhanced acetaminophen toxicity associated with prior alcohol consumption in mice: prevention by N-acetylcysteine.
It is well established that hepatotoxicity is associated with an overdose of acetaminophen and that this hepatotoxicity can be increased by prior alcohol exposure in either humans or animal models. N-Acetylcysteine (NAC) has been developed as a tool to prevent the hepatotoxicity associated with acetaminophen overdosing. The present investigation observed that prior acute and chronic ingestion of alcohol to mice resulted in enhanced toxicity following acetaminophen injection. This increased toxicity was prevented by treatment with NAC. These results suggest that NAC may be a useful tool for combatting the enhanced acetaminophen toxicity associated with alcohol ingestion.
D000082:Acetaminophen / Q000037:antagonists & inhibitors / Q000633:toxicity*; D000111:Acetylcysteine / Q000627:therapeutic use*; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury; D004357:Drug Synergism; D000431:Ethanol / Q000633:toxicity*; D008107:Liver Diseases / Q000517:prevention & control; D008297:Male; D051379:Mice
D000082:Acetaminophen; D000431:Ethanol; D000111:Acetylcysteine