Regular articleThree forms of trichloroethylene-metabolizing enzymes in rat liver induced by ethanol, phenobarbital, and 3-methylcholanthrene
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Toxicity assessments of selected trichloroethylene and perchloroethylene metabolites in three in vitro human placental models
2022, Reproductive ToxicologyCitation Excerpt :It expresses the mRNA of genes that code for enzymes necessary for PERC and TCE glutathione conjugation-derived and cytochrome P450 (CYP) oxidation metabolism [19,20]. These genes include Kyat1 (cysteine conjugate beta-lyase) [21] from the glutathione conjugation pathway and CYP1A1/2 [22,23] from the oxidation pathway. Moreover, the placenta possesses cysteine conjugate beta-lyase activity in rat placenta [24] and human placental cells (data not published), suggesting TCE and PERC metabolites may be in contact with placenta.
Ovarian Metabolism of Xenobiotics
2018, Comprehensive Toxicology: Third EditionTrichloroethylene-induced formic aciduria in the male C<inf>57</inf> Bl/6 mouse
2017, ToxicologyCitation Excerpt :There is however clear evidence of chronic nonneoplastic lesions in the kidney in the carcinogen bioassays, such as renal tubule cytomegaly, karomegaly and toxic nephrosis/nephropathy which occurs in both male and female rats and male and female mice. TCE is primarily metabolised in rodent liver via CYP2E1 (Kim and Ghanayem, 2006), and to a lesser extent by other cytochromes P450 (Nakajima et al., 1990), to form an unstable epoxide which re-arranges to form chloral. CYP2E1 is also present in renal proximal tubules of rats and can metabolise TCE (Cummings et al., 2001) while in mice this isozyme of cytochromes P450 localised in the kidney can activate chloroform and cause renal tubular injury (Smith and Hook, 1984).
Trichloroethylene-induced formic aciduria: Effect of dose, sex and strain of rat
2013, ToxicologyCitation Excerpt :Long term studies have shown an increase in tumour incidence in these tissues, see reviews by Bull (2000), Lock and Reed (2006) and Jollow et al. (2009). TCE is primarily metabolised in the liver via cytochrome P450 2E1 (Kim and Ghanayem, 2006), and to a lesser extent by other cytochromes P450 (Nakajima et al., 1990), to form an unstable epoxide which re-arranges to form chloral. Chloral is then converted to trichloroethanol and its glucuronide and trichloroacetic acid (TCA) which are the major metabolites in the urine of experimental animals and man (Bloemen et al., 2001; Lash et al., 2000; Lock and Reed, 2006).
Proteomic analysis of trichloroethylene-induced alterations in expression, distribution, and interactions of SET/TAF-Iα and two SET/TAF-Iα-binding proteins, eEF1A1 and eEF1A2, in hepatic L-02 cells
2012, Toxicology and Applied PharmacologyCitation Excerpt :TCE-expoxide is then converted to chloral hydrate (CH), which is rapidly metabolized to trichloroacetic acid and trichloroethanol (Cai and Guengerich, 2001; Lash et al., 2000). Of the CYPs involved in TCE hepatic metabolism (Nakajima et al., 1990; Guengerich et al., 1991), CYP2E1 appears to be the major form with the highest affinity for TCE (Nakajima et al., 1992). Patients with TCE intoxication usually suffer liver damage, and the serious consequences of TCE exposure have recently become a critical occupational health issue in China (Kamijima et al., 2007; Kamijima et al., 2008).
Impact of environmental exposures on ovarian function and role of xenobiotic metabolism during ovotoxicity
2012, Toxicology and Applied PharmacologyCitation Excerpt :The CYP isoforms involved in TCE metabolism are CYP1A1/2, CYP2B1/2, CYP2C11/6 and CYP2E1 (Guengerich and Turvy, 1991; Guengerich et al., 1991; Nakajima et al., 1988; 1990; 1992a; 1992b; 1993). Of these isoforms CYP2E1 has the highest affinity for TCE (Cummings and Lash, 2000; Guengerich and Turvy, 1991; Guengerich et al., 1991; Nakajima et al., 1990). In vitro exposure of mouse oocytes to TCAA, DCA and TCOH also reduces fertilization rates (Cosby and Dukelow, 1992) and has been detected in the rat ovary following TCE exposure through drinking water (0.45% for 2 weeks; Wu and Berger, 2007).