Abstract
Acetaminophen (ACET) is a common analgesic and antipyretic drug that in excessive concentrations may cause acute liver damage and acute renal failure (1). Although the normal elimination of ACET seems to involve conjugation of a toxic alkylating metabolite with liver glutathione to yield a detoxified conjugation product, excessive doses of ACET deplete liver glutathione stores, causing accumulation of the toxic metabolite N -acetyl-imidoquinone (1)(2)(3). Acetylcysteine (NAC, N -acetyl-3-mercaptoalanine) is the drug of choice for the treatment of an ACET overdose. Although the mechanism responsible for the ability of NAC to serve as an effective antidote in vivo has not been fully elucidated, a major route of detoxification seems to depend on the ability of NAC to serve as a potent sulfhydryl donor that restores depleted …
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