ACETAMINOPHEN-INDUCED HEPATOTOXICITY¶
James, Mayeux, & Hinson. (2003). ACETAMINOPHEN-INDUCED HEPATOTOXICITY. Drug Metabolism and Disposition.
Cited by¶
1 citation across 1 artifact.
Each citation links to the sentence it supports in the citing article.
Domain-specific¶
- Elimination Pathway
- At therapeutic doses the great majority of the drug is cleared by Phase II conjugation — glucuronidation and sulfation — to harmless water-soluble metabolites, while a small fraction is oxidized by the CYP2E1 enzyme to a reactive intermediate, NAPQI
This sourceReview of acetaminophen hepatotoxicity establishing that P450-mediated metabolic activation yields the reactive metabolite NAPQI, which depletes glutathione.
Supported in partVerified against a saved copy of the source
“These findings indicated that acetaminophen was metabolically activated by cytochrome P450 enzymes to a reactive metabolite that depleted glutathione (GSH) and covalently bound to protein.”
- At therapeutic doses the great majority of the drug is cleared by Phase II conjugation — glucuronidation and sulfation — to harmless water-soluble metabolites, while a small fraction is oxidized by the CYP2E1 enzyme to a reactive intermediate, NAPQI
Verification¶
Does it exist? Not checked yet. This work's DOI is recorded above but has not been resolved against an external catalogue, so nothing here confirms the work exists.
Does it back the claim? Read against the text for 1 of 1 citation: 1 supported in part. Each verdict is shown under its citation below, with what in the work backs the sentence.
Support is checked per citation rather than per work — the same source can be cited soundly in one article and wrongly in another. Per-citation recording began recently, so a citation with no recorded check is a gap in the record rather than evidence it went unchecked.
See how references were verified.
Registry ID ref:3a91b670f05b · see in the full table