Fundamental and Applied Toxicology
Regular ArticleTrichloroethylene-Induced Mouse Lung Tumors: Studies of the Mode of Action and Comparisons between Species☆
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Apoptotic responses stimulated by the trichloroethylene metabolite S-(1,2-dichlorovinyl)-L-cysteine depend on cell differentiation state in BeWo human trophoblast cells
2023, Toxicology in VitroCitation Excerpt :This finding highlights that DCVC toxicity changes with cell status at DCVC concentrations similar to effective concentrations in BeWo, whether it is differentiation state as seen in the present study or passage number as reported by Lash et al.. Differences in response to DCVC that are dependent on differentiation state may have relevance to TCE toxicity to various organs, including kidney (Green et al., 1997a; Xu et al., 2008; Lash et al., 2014b), liver (Bull, 2000), and lungs (Forkert et al., 1985; Green et al., 1997b), with respect to sensitive cell populations. BeWo cell models have strengths as well as limitations.
Evaluation of the carcinogenicity of dichloromethane in rats, mice, hamsters and humans
2021, Regulatory Toxicology and PharmacologyCitation Excerpt :While a mutagenic mode of action in mice is supported by the mutagenicity of DCM in bacteria (expressing the specific glutathione S-transferases) and some positive assays for genotoxicity following inhalation exposure in vivo, even the database on the genotoxicity of DCM in mice remains inconsistent since higher tier genotoxicity assays with DCM in mice are negative and an assessment of genomic changes in mice exposed by inhalation up to 4000 ppm DCM for 90 days did not show a DNA-damage response in lung and liver (Andersen et al., 2017). Moreover, mice are generally sensitive to lung (and liver) tumor induction by chemicals through non-genotoxic modes of action (Green et al., 1997; Banton et al., 2019; Cohen et al., 2020) and a wide range of chemicals can cause cancer under the “right” experimental circumstances many of which having no relevance to humans or achievable exposure levels (Boobis et al., 2016). It is, however, clear that rats and hamsters did not show tumors in response to DCM concentrations up to 4000 ppm, and genotoxicity testing of DCM in these species overall gave negative results.
Metabolism of 4-methylimidazole in Fischer 344 rats and B6C3F1 mice
2019, Food and Chemical ToxicologyCitation Excerpt :In mice, the exocrine bronchiolar cell or club cell, the primary location of CYP enzymes in the lungs, is present in much greater numbers than in rats, and in turn in human lung, (Plopper et al., 1980a; b; Plopper et al., 1992), resulting in substantially higher metabolism in the mouse lung compared to the rat lung. For example, trichloroethylene undergoes more extensive oxidation in mouse lung than rat lung via CYP2E1 expressed in mouse lung club cells (Green et al., 1997). Methylene chloride undergoes extensive metabolism via glutathione transferase theta in mouse lung compared with rat lung, and this is thought to be a key difference in the response difference between rat and mouse (Green, 1997).
Trichloroethylene: Mechanistic, epidemiologic and other supporting evidence of carcinogenic hazard
2014, Pharmacology and TherapeuticsCitation Excerpt :Smoking, but not solvent exposure, was shown as a statistically significant predictor of lung function decrements. Acute cytotoxicity in the bronchiolar Clara cell and transient cell proliferation following TCE exposure were observed in mouse studies (Villaschi et al., 1991; Forkert & Forkert, 1994; Buckpitt et al., 1995; Green et al., 1997b). In sub-chronic studies, pulmonary fibrosis was observed 90 days following i.p. administration of a single dose of TCE (Forkert & Forkert, 1994).
Development and evaluation of a harmonized physiologically based pharmacokinetic (PBPK) model for perchloroethylene toxicokinetics in mice, rats, and humans
2011, Toxicology and Applied PharmacologyCitation Excerpt :The ratio of the renal to hepatic Km in tissue concentration units is assumed to be 1 (converted to Km in venous blood by using the liver–blood and kidney–blood partition coefficients). There are no available data on lung oxidation of perc, so the ratio of lung to liver oxidation for TCE from Green et al. (1997) is used. The ratio of the lung to hepatic Km in tissue concentration units (i.e., adjusted using liver–blood and lung–blood partition coefficients) is assumed to be 1, which is then converted to Km in air (in the lumen) by using the blood–air partition coefficients.