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[edit] Summary

Schematic of the metabolism of acetaminophen (paracetamol) by the hepatocyte. Acetaminophen is predominantly conjugated into glucuronate and sulfate moieties by Phase II metabolism. A small percentage is metabolized by the cytochrome P450 pathway to a toxic metabolite, NAPQI. NAPQI is conjugated by glutathione to non-toxic cysteine and mercapturic acid moieties. In cases of acetaminophen toxicity, the Phase II conjugation enzymes are saturated, and a higher fraction is converted to NAPQI. The conjugation of NAPQI to glutahtione occurs until glutathione is depleted from hepatic reserves, after which the toxic NAPQI accumulates and causes damage to the hepatocytes. N-acetylcysteine or NAC is a glutathione precursor and functions by repleting glutathione stores. Alcoholics are particularly susceptible to acetaminophen toxicity as the P450 enzymes are upregulated in the setting of chronic alcohol use. -- Samir धर्म 08:44, 15 September 2006 (UTC)

[edit] Licensing

I, the creator of this work, hereby grant the permission to copy, distribute and/or modify this document under the terms of the GNU Free Documentation License, Version 1.2 or any later version published by the Free Software Foundation; with no Invariant Sections, no Front-Cover Texts, and no Back-Cover Texts. Subject to disclaimers.

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	Date/Time	Dimensions	User	Comment
current	08:44, 15 September 2006	865×621 (43 KB)	Samir (Talk \| contribs)	(Schematic of the metabolism of acetaminophen (paracetamol) by the hepatocyte. Acetaminophen is predominantly conjugated into glucuronate and sulfate moieties by Phase II metabolism. A small percentage is metabolized by the [[cytochrome P)