ArticleToxicological sciences : an official journal of the Society of Toxicology2016
Vinyl Chloride Metabolites Potentiate Inflammatory Liver Injury Caused by LPS in Mice.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
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- Association between volatile organic compounds exposure and cardiometabolic function: a population-based study.Frontiers in public health · 2025Article
- Environmental pollutants and phosphoinositide signaling in autoimmunity.Journal of hazardous materials · 2024Review
- Effects of Dietary Ferulic Acid on Intestinal Health and Ileal Microbiota of Tianfu Broilers Challenged with Lipopolysaccharide.Molecules (Basel, Switzerland) · 2023Article
- Protective role of selenium on structural change of human hemoglobin in the presence of vinyl chloride.Toxicological research · 2022Article
- Environmental Toxicants and NAFLD: A Neglected yet Significant Relationship.Digestive diseases and sciences · 2022Review
- Thymol Alleviates LPS-Induced Liver Inflammation and Apoptosis by Inhibiting NLRP3 Inflammasome Activation and the AMPK-mTOR-Autophagy Pathway.Nutrients · 2022Article
- Role of Climate Change in Changing Hepatic Health Maps.Current environmental health reports · 2022Review
- Effect of vinyl chloride exposure on cardiometabolic toxicity.Environmental toxicology · 2022Article
- Volatile organic compounds: A proinflammatory activator in autoimmune diseases.Frontiers in immunology · 2022Review
- Environmental toxicant-induced maladaptive mitochondrial changes: A potential unifying mechanism in fatty liver disease?Acta pharmaceutica Sinica. B · 2021Review
- Plasma Metabolomics Analysis of Polyvinyl Chloride Workers Identifies Altered Processes and Candidate Biomarkers for Hepatic Hemangiosarcoma and Its Development.International journal of molecular sciences · 2021Article
- A Novel Function of Mitochondrial Phosphoenolpyruvate Carboxykinase as a Regulator of Inflammatory Response in Kupffer Cells.Frontiers in cell and developmental biology · 2021Article
- Associations of soluble metals and lung and liver toxicity in mice induced by fine particulate matter originating from a petrochemical complex.Environmental science and pollution research international · 2020Article
- Adipose tissue-liver crosstalk during pathologic changes caused by vinyl chloride metabolites in mice.Toxicology and applied pharmacology · 2020Article
- Hepatic Injury Caused by the Environmental Toxicant Vinyl Chloride is Sex-Dependent in Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Vinyl Chloride and High-Fat Diet as a Model of Environment and Obesity Interaction.Journal of visualized experiments : JoVE · 2020Article
- Rapamycin attenuates liver injury caused by vinyl chloride metabolite chloroethanol and lipopolysaccharide in mice.Toxicology and applied pharmacology · 2019Article
- Mechanisms of Environmental Contributions to Fatty Liver Disease.Current environmental health reports · 2019Review
- Vinyl chloride-induced interaction of nonalcoholic and toxicant-associated steatohepatitis: Protection by the ALDH2 activator Alda-1.Redox biology · 2019Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Vinyl chloride (VC) is a ubiquitous environmental contaminant for which human risk is incompletely understood. We have previously reported that high occupational exposure to VC directly caused liver damage in humans. However, whether VC may also potentiate liver injury from other causes is not known. C57Bl/6J mice were administered chloroethanol (CE), a major metabolite of VC, and lipopolysaccharide (LPS) 24 h after CE. Samples were harvested for determination of liver damage, inflammation, and changes in carbohydrate and lipid metabolism. In mice, CE exposure alone caused no detectable liver damage. LPS exposure caused inflammatory liver damage, oxidative stress, lipid accumulation, and glycogen depletion; the effect of all of these variables was potentiated by CE pre-exposure. In vitro experiments suggest that VC metabolite chloroacetaldehyde (CAA) directly damages mitochondria, which may explain the sensitization effect observed in vivo Moreover, co-exposure of cells to CAA and TNFα caused increased cell death, supporting the hypothesis of sensitization by VC metabolites. Taken together, these data demonstrate that exposure to VC/metabolites at levels that are not overtly hepatotoxic can potentiate liver injury caused by another hepatotoxicant. This serves as proof-of-concept that VC hepatotoxicity may be modified by an additional metabolic stress such as endotoxemia, which commonly occurs in acute (eg, sepsis) and chronic (eg, NAFLD) diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.