Regular ArticleIn Vivoandin VitroStudies of Perchloroethylene Metabolism for Physiologically Based Pharmacokinetic Modeling in Rats, Mice, and Humans
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Incorporation of the glutathione conjugation pathway in an updated physiologically-based pharmacokinetic model for perchloroethylene in mice
2018, Toxicology and Applied PharmacologyCitation Excerpt :In vivo data for B6C3F1 and SW strains were reviewed thoroughly and used in the previous perc PBPK model (Chiu and Ginsberg, 2011). Studies in B6C3F1 mice included inhalation, closed chamber and oil gavage administration at a range of exposure levels, and reported perc and its oxidative metabolite, TCA, in blood (Gargas, 1988; Odum et al., 1988; Gearhart et al., 1993; Reitz et al., 1996). Only data using aqueous gavage of perc was available for the SW strain, reporting concentrations of perc in blood, liver and kidney, and its oxidative metabolite, TCA, in blood and liver (Philip et al., 2007).
Halogenated Hydrocarbons
2018, Comprehensive Toxicology: Third EditionDevelopment and evaluation of a harmonized physiologically based pharmacokinetic (PBPK) model for perchloroethylene toxicokinetics in mice, rats, and humans
2011, Toxicology and Applied PharmacologyCitation Excerpt :For rat calibration data, the poorest fits are to the fraction of retained perc metabolized and rate of perc exhalation (both from Reitz et al., 1996) and perc in various tissues (from Dallas et al., 1994a, 1994c; and Warren et al., 1996), with residual errors of 2- to 3-fold. As with mice, it is unclear how to completely reconcile the extremely well-fit closed chamber data with the more poorly fit C-14 data from Reitz et al. (1996), but inter-study variation cannot be ruled out. All the remaining data have more modest (< 2-fold) residual errors.