Role of lipid peroxidation in renal proximal tubule cell death induced by haloalkene cysteine conjugates☆
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The trichloroethylene metabolite S-(1,2-dichlorovinyl)-L-cysteine induces progressive mitochondrial dysfunction in HTR-8/SVneo trophoblasts
2019, ToxicologyCitation Excerpt :These results suggest an exposure duration threshold of 12 h for 20 μM DCVC-induced mitochondrial membrane depolarization. Due to evidence of reactive oxygen species and lipid peroxidation involvement in the toxicological mechanism for DCVC-mediated toxicity in placental and kidney cells (Beuter et al. 1989; Chen et al., 1990; Elkin et al., 2018; Groves et al., 1991; Hassan et al., 2016), the role of lipid peroxidation in DCVC-induced mitochondrial perturbations was evaluated by including treatment with (±)α-tocopherol, an antioxidant that blocks lipid peroxidation (Horwitt, 1986). Co-treatment with 50 μM (±)α-tocopherol significantly rescued mitochondrial membrane depolarization caused by 20 μM DCVC exposure for 12 h (Fig. 4A; P < 0.001).
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2018, Comprehensive Toxicology: Third EditionTrichloroethylene metabolite S-(1,2-dichlorovinyl)-L-cysteine induces lipid peroxidation-associated apoptosis via the intrinsic and extrinsic apoptosis pathways in a first-trimester placental cell line
2018, Toxicology and Applied PharmacologyCitation Excerpt :We found that DCVC treatment increased malondialdehydes in HTR-8/SVneo cells, a byproduct and proxy measure for lipid peroxidation. These results are consistent with previous studies that indicate DCVC causes lipid peroxidation in kidney tubular cells of humans and rodents (Beuter et al., 1989; Chen et al., 1990; Groves et al., 1991). Lipid peroxidation occurs when reactive oxygen species, including free radicals, attack carbon double bonds in lipids resulting in lipid peroxyl radicals and hydroperoxides (Ayala et al., 2014).
Renal Organic Ion Transport
2013, In Vitro Toxicity IndicatorsEnzymes Involved in Processing Glutathione Conjugates
2010, Comprehensive Toxicology, Second EditionHalogenated Hydrocarbons
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This work was supported in part by National Institutes of Health Grant ES-04410. R.G.S. is a recipient of a PMA Foundation Faculty Development Award. C.E.G. is a recipient of a PMA Foundation Predoctoral Fellowship.