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Interaction between acetaminophen and organophosphates in mice.

L G Costa, S D Murphy

    Research Communications in Chemical Pathology and Pharmacology
    |June 1, 1984
    PubMed
    Summary

    Acetaminophen depletes liver sulfhydryls but does not increase organophosphate toxicity. However, diethylmaleate does, suggesting extrahepatic glutathione is crucial for detoxifying some organophosphates.

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    Area of Science:

    • Biochemistry
    • Toxicology
    • Pharmacology

    Background:

    • Organophosphates are detoxified by glutathione transferases.
    • Hepatic nonprotein sulfhydryls (NPSH) play a role in detoxification pathways.
    • Acetaminophen is known to deplete hepatic NPSH.

    Purpose of the Study:

    • To investigate if acetaminophen-induced depletion of hepatic NPSH potentiates organophosphate toxicity.
    • To compare the effects of acetaminophen and diethylmaleate on NPSH levels and organophosphate toxicity.

    Main Methods:

    • Mice were administered acetaminophen or diethylmaleate to deplete hepatic NPSH.
    • Organophosphate insecticides (methylchlorpyrifos, methylparathion, dichlorvos) were administered.
    • Esterase inhibition and toxicity were measured.

    Main Results:

    • Acetaminophen depleted hepatic NPSH but did not potentiate organophosphate toxicity.
    • Diethylmaleate depleted NPSH in multiple tissues and increased organophosphate toxicity.
    • Acetaminophen's inhibition of mixed function oxidase may affect metabolism of some organophosphates.

    Conclusions:

    • Hepatic NPSH depletion by acetaminophen does not enhance organophosphate toxicity.
    • Extrahepatic glutathione may be important for detoxifying certain organophosphates.
    • Mechanisms beyond hepatic NPSH depletion are involved in acetaminophen's interaction with organophosphate toxicity.

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