ArticleBiochemical pharmacology2008
Role of mitochondrial dysfunction in cellular responses to S-(1,2-dichlorovinyl)-L-cysteine in primary cultures of human proximal tubular cells.
Article in Biochemical pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Perturbation of metabolic pathways associated with exposure of human renal proximal tubular cells to nephrotoxic pollutants and drugs.Toxicology · 2026Article
- Neurotoxicology of dopamine: Victim or assailant?Neurotoxicology · 2024Review
- Article
- Trichloroethylene MetaboliteChemical research in toxicology · 2023Article
- Apoptotic responses stimulated by the trichloroethylene metabolite S-(1,2-dichlorovinyl)-L-cysteine depend on cell differentiation state in BeWo human trophoblast cells.Toxicology in vitro : an international journal published in association with BIBRA · 2023Article
- Article
- The trichloroethylene metabolite S-(1,2-dichlorovinyl)-l-cysteine inhibits lipopolysaccharide-induced inflammation transcriptomic pathways and cytokine secretion in a macrophage cell model.Toxicology in vitro : an international journal published in association with BIBRA · 2022Article
- Toxicity assessments of selected trichloroethylene and perchloroethylene metabolites in three in vitro human placental models.Reproductive toxicology (Elmsford, N.Y.) · 2022Article
- Mapping Adverse Outcome Pathways for Kidney Injury as a Basis for the Development of Mechanism-Based Animal-Sparing Approaches to Assessment of Nephrotoxicity.Frontiers in toxicology · 2022Article
- Transcriptional profiling of the response to the trichloroethylene metabolite S-(1,2-dichlorovinyl)-L-cysteine revealed activation of the eIF2α/ATF4 integrated stress response in two in vitro placental models.Archives of toxicology · 2021Article
- Diverse Roles of Mitochondria in Renal Injury from Environmental Toxicants and Therapeutic Drugs.International journal of molecular sciences · 2021Review
- Renal proximal tubular epithelial cells: review of isolation, characterization, and culturing techniques.Molecular biology reports · 2020Review
- Exposure to Trichloroethylene MetaboliteChemical research in toxicology · 2020Article
- Trichloroethylene, a ubiquitous environmental contaminant in the risk for Parkinson's disease.Environmental science. Processes & impacts · 2020Article
- The trichloroethylene metabolite S-(1,2-dichlorovinyl)-L-cysteine induces progressive mitochondrial dysfunction in HTR-8/SVneo trophoblasts.Toxicology · 2019Article
- Trichloroethylene exposure in mid-pregnancy decreased fetal weight and increased placental markers of oxidative stress in rats.Reproductive toxicology (Elmsford, N.Y.) · 2019Article
- Trichloroethylene 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.Toxicology and applied pharmacology · 2018Article
- Reactive Oxygen Stimulation of Interleukin-6 Release in the Human Trophoblast Cell Line HTR-8/SVneo by the Trichlorethylene Metabolite S-(1,2-Dichloro)-l-Cysteine.Biology of reproduction · 2016Article
- Hesperidin ameliorates trichloroethylene-induced nephrotoxicity by abrogation of oxidative stress and apoptosis in wistar rats.Molecular and cellular biochemistry · 2015Article
- The trichloroethylene metabolite S-(1,2-dichlorovinyl)-l-cysteine but not trichloroacetate inhibits pathogen-stimulated TNF-α in human extraplacental membranes in vitro.Reproductive toxicology (Elmsford, N.Y.) · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The nephrotoxic metabolite of the environmental contaminant trichloroethylene, S-(1,2-dichlorovinyl)-l-cysteine (DCVC), is known to elicit cytotoxicity in rat and human proximal tubular (rPT and hPT, respectively) cells that involves inhibition of mitochondrial function. DCVC produces a range of cytotoxic and compensatory responses in hPT cells, depending on dose and exposure time, including necrosis, apoptosis, repair, and enhanced cell proliferation. The present study tested the hypothesis that induction of mitochondrial dysfunction is an obligatory step in the cytotoxicity caused by DCVC in primary cultures of hPT cells. DCVC-induced necrosis was primarily a high concentration (> or =50 microM) and late (> or =24h) response whereas apoptosis and increased proliferation occurred at relatively low concentrations (<50 microM) and early time points (< or =24h). Decreases in cellular DNA content, indicative of cell loss, were observed at DCVC concentrations as low as 1 microM. Involvement of mitochondrial dysfunction in DCVC-induced cytotoxicity was supported by showing that DCVC caused modest depletion of cellular ATP, inhibition of respiration, and activation of caspase-3/7. Cyclosporin A protected cells against DCVC-induced apoptosis and both cyclosporin A and ruthenium red protected cells against DCVC-induced loss of mitochondrial membrane potential. DCVC caused little or no activation of caspase-8 and did not significantly induce expression of Fas receptor, consistent with apoptosis occurring only by the mitochondrial pathway. These results support the conclusion that mitochondrial dysfunction is an early and obligatory step in DCVC-induced cytotoxicity in hPT cells.
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Registered trials
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