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- W137672807 abstract "Acetaminophen (APAP) overdose is the leading cause of acute liver failure in the U.S. Cytochromes P450 CYP2E1, CYP1A2, and CYP3A4 have all been implicated in formation of the reactive intermediate of APAP, and thus can contribute to APAP hepatotoxicity. The nuclear pregnane X receptor (PXR) plays a critical role in CYP3A regulation and many drugs and dietary compounds are PXR activators. Thus, it is important to determine whether PXR-mediated CYP3A induction is a risk factor for APAP hepatotoxicity. In this study, a double transgenic human PXR and CYP3A4 mice (TgCYP3A4/hPXR) mouse model was generated in a mouse Pxr-null background. In this model, CYP3A4 was strongly induced by rifampicin (RIF), a human-specific PXR ligand, but not by pregnenolone 16α-carbonitrile, a rodent-specific PXR ligand. Consistent with CYP3A4 expression, hepatic CYP3A4 activity increased ~500% in TgCYP3A4/hPXR mice treated with RIF. However, APAP (250 mg/kg, p.o.) hepatotoxicity did not concurrently increase in TgCYP3A4/hPXR mice upon PXR activation and CYP3A4 induction, as revealed by hepatic histological changes and serum ALT levels. Moreover, there were no significant differences in the major APAP urinary metabolites between RIF-pretreated and vehicle-treated groups. In conclusion, these studies suggest that PXR-mediated CYP3A4 induction does not enhance APAP hepatotoxicity and PXR ligands are not risk factors for hepatotoxicity when combined medication with APAP." @default.
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- W137672807 date "2007-01-01" @default.
- W137672807 modified "2023-09-27" @default.
- W137672807 title "The effect of pregnane X receptor (PXR)‐mediated CYP3A induction on acetaminophen hepatotoxicity" @default.
- W137672807 doi "https://doi.org/10.1096/fasebj.21.6.a1184-d" @default.
- W137672807 hasPublicationYear "2007" @default.
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