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Acetaminophen and its toxicity.

M C Savides, F W Oehme

    Journal of Applied Toxicology : JAT
    |April 1, 1983
    PubMed
    Summary

    Acetaminophen (APAP) overdose causes liver and kidney damage by depleting glutathione. Treatment involves providing alternative sulfhydryl donors or inhibiting reactive metabolite formation, with plasma APAP level monitoring crucial for effective management.

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    Area of Science:

    • Pharmacology
    • Toxicology
    • Hepatology

    Background:

    • Acetaminophen (APAP) is a widely used analgesic, generally safe at therapeutic doses.
    • High doses (over 10 g) of APAP can lead to severe hepatotoxicity and nephrotoxicity.
    • APAP metabolism involves major conjugation pathways and a minor pathway producing a reactive metabolite.

    Purpose of the Study:

    • To review the metabolic pathways of acetaminophen.
    • To understand the mechanism of acetaminophen-induced toxicity.
    • To outline current treatment strategies for acetaminophen poisoning.

    Main Methods:

    • Literature review of acetaminophen metabolism and toxicity.
    • Analysis of biochemical pathways involved in APAP detoxification and activation.
    • Summary of clinical management protocols for APAP overdose.

    Main Results:

    • The primary metabolic routes for APAP are glucuronidation and sulfation.
    • A minor metabolic pathway generates a reactive electrophilic metabolite.
    • Glutathione (GSH) depletion by this reactive metabolite leads to hepatocellular necrosis.
    • Severe poisoning results in hepatic and/or renal failure.

    Conclusions:

    • Acetaminophen toxicity is mediated by a reactive metabolite that depletes GSH.
    • Treatment strategies focus on replenishing GSH or inhibiting the formation of the toxic metabolite.
    • Monitoring plasma APAP concentrations is essential for guiding treatment decisions.

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