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Acetylcysteine is extensively liver metabolized, CYP450 minimal, urine excretion is 22–30% with a half-life of 5.6 hours in adults and 11 hours in newborns. [medical citation needed] Acetylcysteine is the N-acetyl derivative of the amino acid L-cysteine, and is a precursor in the formation of the antioxidant glutathione in the body.
Acetylcysteine is the antidote for paracetamol toxicity. Acetylcysteine, also called N-acetylcysteine or NAC, works to reduce paracetamol toxicity by replenishing body stores of the antioxidant glutathione. Glutathione reacts with the toxic NAPQI metabolite so that it does not damage cells and can be safely excreted. [67]
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.
"Standard preparations of green tea are less likely to cause liver toxicity," Dr. David ... adding, "Most cases of hepatotoxicity resolve spontaneously or with the administration of acetylcysteine."
The Rumack–Matthew nomogram, also known as the acetaminophen nomogram, is an acetaminophen toxicity nomogram. It plots serum concentration of acetaminophen against the time since ingestion, in order to predict possible liver toxicity and allow a clinician to decide whether to proceed with N-Acetylcysteine (NAC) treatment.
Hepatotoxicity (from hepatic toxicity) implies chemical-driven liver damage. Drug-induced liver injury (DILI) is a cause of acute and chronic liver disease caused specifically by medications and the most common reason for a drug to be withdrawn from the market after approval.
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