NAPQI, also known as NAPBQI or N-acetyl-p-benzoquinone imine, is a toxic byproduct produced during the xenobiotic metabolism of the analgesic paracetamol (acetaminophen). [1] It is normally produced only in small amounts, and then almost immediately detoxified in the liver.

The principal toxic metabolite of acetaminophen, N-acetyl-p-benzoquinone imine (NAPQI), is produced by the hepatic cytochrome P-450 enzyme system; glutathione stores in the liver detoxify this metabolite. An acute overdose depletes glutathione stores in the liver.

N-Acetyl-p-benzoquinone imine (NAPQI), a reactive metabolite of acetaminophen, rapidly reacts at physiological pH with glutathione (GSH) forming an acetaminophen-glutathione conjugate and stoichiometric amounts of acetaminophen and glutathione disulfide (GSSG).

Inhibition of glutathione synthetase (GS) by N-acetyl-p-benzoquinone imine (NAPQI) could contribute to 5-oxoprolinuric acidosis in such patients. We investigated the interaction of NAPQI with GS in vitro.

Acetaminophen is the leading cause of acute hepatic failure in many developed nations. Acetaminophen hepatotoxicity is mediated by the reactive metabolite N-acetyl-p-benzoquinonimine (NAPQI). We performed a “discovery” genome-wide association study ...

Overdose will lead to excess NAPQI, which depletes glutathione supply, and reactive intermediates damage hepatocytes. N-acetylcysteine (NAC, Mucomyst®) works by repleting glutathione, enhancing sulfate conjugation, and may directly bind to NAPQI.

Severe liver toxicity (peak AST or ALT >1000 IU/L) develops in virtually all patients who ingest doses in excess of 350 mg/kg. Normal metabolism: supratherapeutic doses (>4g) lead to oxidation to a reactive intermediate (NAPQI) and glutathione depletion. NAPQI binds to cellular proteins, leading to hepatocyte necrosis.

2017年5月4日 · Acetaminophen (Tylenol) is typically metabolized into nontoxic products by means of sulfation and glucoronidation (blue and green paths, respectively). A small percentage undergoes metabolism into NAPQI, a TOXIC metabolite, via the CYP enzyme family (red).

N-acetyl-p-benzoquinone imine (NAPQI) has been proposed as the toxic metabolite of acetaminophen for the past 10 years, although it has never been detected as an enzymatic oxidation product of acetaminophen. We report (i) direct detection of NAPQI ...

The breakdown product, N-acetyl-p-benzo-quinone imine; NAPQI) reacts with the sulphydryl groups of glutathione, which are used up by the excessive amount of breakdown product. When the glutathione is completely used up, the NAPQI begins to react with liver cell proteins, killing the cells. It causes necrosis in the liver cells and kidney tubules.