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  • Title: Metabolic activation of phosphorothioate pesticides: role of the liver.
    Author: Sultatos LG, Minor LD, Murphy SD.
    Journal: J Pharmacol Exp Ther; 1985 Mar; 232(3):624-8. PubMed ID: 2579231.
    Abstract:
    Mouse liver perfusion studies in situ revealed that the cholinesterase inhibitor chlorpyrifos oxon produced by the liver from the phosphorothioate pesticide chlorpyrifos was quickly detoxified within the liver, thereby preventing it's exit from the liver in the effluent. In contrast, when the pesticide parathion was perfused as a substrate a substantial amount of the toxic metabolite paraoxon was found in exiting perfusate. Pesticide concentrations (5-15 microM) used in the perfusion studies in situ were similar to their hepatic portal blood concentrations in vivo (2.32-12.95 microM) after i.p. administration of lethal or near lethal doses. Moreover, the half-life for elimination of paraoxon by mouse blood in vitro was 8.6 min, a rate sufficiently low to allow passage of paraoxon to extrahepatic target tissues from liver in vivo. These results suggest that in the mouse, the acute toxicity of chlorpyrifos is mediated by extrahepatic production of oxon, whereas that of parathion is likely mediated by both hepatic and extrahepatic activation.
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