Lung injury induced by trichloroethylene
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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.
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2018, Comprehensive Toxicology: Third EditionOccupational health hazards of trichloroethylene among workers in relation to altered mRNA expression of cell cycle regulating genes (p53, p21, bax and bcl-2) and PPARA
2015, Toxicology ReportsCitation Excerpt :The exposure to TCE can lead to bronchiolar damage in workers. In the rodent model, TCE was observed to produce bronchiolar damage when administered to mice [30]. TCE is carcinogenic to the mouse lung and the toxicity is confined to the accumulation of TCE metabolite in non-ciliated Clara cells of the lung.
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2010, Comprehensive Toxicology, Second Edition