re deadly nyquil in article c bk f h i murdoch acc virginia edu res w galen med virginia edu robert e schmieg writes partial deletion potentially fatal from hepatic necrosis if i recall correctly the metabolism of acetaminophen at high doses involves n hydroxylation to n acetyl benzoquinoneimine which is a highly reactive intermediate which then reacts with sulfhydryl groups of proteins and glutathione when hepatic glutathione is used up this intermediate then starts attacking the hepatic proteins with resulting hepatic necrosis the insidious part of acetaminophen toxicity is the delay days between ingestion and clinical signs of liver damage this is not a nice way to die nice explanation except that it isn t n hydroxylation that causes the formation of the n acetyl p benzoquinone imine napqi but rather a direct two electron oxidation in addition there is one school of thought that contends that oxidative stress rather than arylation of protein is the more critical factor in the hapatotoxcity of acetaminophen as far as drug toxicities go acetaminophen has and continues to be one of the most intensely scrutinized an excellent recent review of the topic can be found in vermeulen bessems and van de straat molecular aspects of paracetamol induced hepatotoxicity and its mechanism based prevention drug metabolism reviews acetaminophen is known as paracetamol in europe i couldn t agree with you more about what an awful way to die a toxic dose of acetaminophen causes i ve heard a number of descriptions by physicians associated with poison control centers and they describe a lingering very painful death gary
