ArticleArchives of toxicology2013
Metabolomics reveals trichloroacetate as a major contributor to trichloroethylene-induced metabolic alterations in mouse urine and serum.
Article in Archives of toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Lipidomics reveal aryl hydrocarbon receptor (Ahr)-regulated lipid metabolic pathway in alpha-naphthyl isothiocyanate (ANIT)-induced intrahepatic cholestasis.Xenobiotica; the fate of foreign compounds in biological systems · 2019Article
- Protective Effect ofInternational journal of molecular sciences · 2018Article
- Glycyrrhizin and glycyrrhetinic acid inhibits alpha-naphthyl isothiocyanate-induced liver injury and bile acid cycle disruption.Toxicology · 2017Article
- Editor's Highlight: Collaborative Cross Mouse Population Enables Refinements to Characterization of the Variability in Toxicokinetics of Trichloroethylene and Provides Genetic Evidence for the Role of PPAR Pathway in Its Oxidative Metabolism.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Role of the lipid-regulated NF-κB/IL-6/STAT3 axis in alpha-naphthyl isothiocyanate-induced liver injury.Archives of toxicology · 2017Article
- High-resolution metabolomics of occupational exposure to trichloroethylene.International journal of epidemiology · 2016Article
- Irinotecan (CPT-11)-induced elevation of bile acids potentiates suppression of IL-10 expression.Toxicology and applied pharmacology · 2016Article
- Metabolic mapping of A3 adenosine receptor agonist MRS5980.Biochemical pharmacology · 2015Article
- Regulation profile of phosphatidylcholines (PCs) and lysophosphatidylcholines (LPCs) components towards UDP-glucuronosyltransferases (UGTs) isoforms.Xenobiotica; the fate of foreign compounds in biological systems · 2015Article
- LC-MS-based metabolomics: an update.Archives of toxicology · 2014Review
- Gemfibrozil disrupts lysophosphatidylcholine and bile acid homeostasis via PPARα and its relevance to hepatotoxicity.Archives of toxicology · 2014Article
- Do Antioxidant Enzymes and Glutathione Play Roles in the Induction of Hepatic Oxidative Stress in Mice upon Subchronic Exposure to Mixtures of Dichloroacetate and Trichloroacetate?Toxicological and environmental chemistry · 2014Article
- An integrative model of multi-organ drug-induced toxicity prediction using gene-expression data.BMC bioinformatics · 2014Article
- The effects of mixtures of dichloroacetate and trichloroacetate on induction of oxidative stress in livers of mice after subchronic exposure.Journal of toxicology and environmental health. Part A · 2014Article
- Environmental pollution: a tangible risk for NAFLD pathogenesis.International journal of molecular sciences · 2013Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Trichloroethylene (TCE)-induced liver toxicity and carcinogenesis is believed to be mediated in part by activation of the peroxisome proliferator-activated receptor α (PPARα). However, the contribution of the two TCE metabolites, dichloroacetate (DCA) and trichloroacetate (TCA) to the toxicity of TCE, remains unclear. The aim of the present study was to determine the metabolite profiles in serum and urine upon exposure of mice to TCE, to aid in determining the metabolic response to TCE exposure and the contribution of DCA and TCA to TCE toxicity. C57BL/6 mice were administered TCE, TCA, or DCA, and urine and serum subjected to ultra-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight mass spectrometry (UPLC-ESI-QTOFMS)-based global metabolomics analysis. The ions were identified through searching metabolomics databases and by comparison with authentic standards, and quantitated using multiple reactions monitoring. Quantitative polymerase chain reaction of mRNA, biochemical analysis, and liver histology were also performed. TCE exposure resulted in a decrease in urine of metabolites involved in fatty acid metabolism, resulting from altered expression of PPARα target genes. TCE treatment also induced altered phospholipid homeostasis in serum, as revealed by increased serum lysophosphatidylcholine 18:0 and 18:1, and phosphatidylcholine metabolites. TCA administration revealed similar metabolite profiles in urine and serum upon TCE exposure, which correlated with a more robust induction of PPARα target gene expression associated with TCA than DCA treatment. These data show the metabolic response to TCE exposure and demonstrate that TCA is the major contributor to TCE-induced metabolite alterations observed in urine and serum.
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