ArticleToxicology and applied pharmacology2016
Role of dietary fatty acids in liver injury caused by vinyl chloride metabolites in mice.
Article in Toxicology and applied pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- The application of natural language processing for the extraction of mechanistic information in toxicology.Frontiers in toxicology · 2024Article
- 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
- Adipose tissue-liver crosstalk during pathologic changes caused by vinyl chloride metabolites in mice.Toxicology and applied pharmacology · 2020Article
- Blood BTEXS and heavy metal levels are associated with liver injury and systemic inflammation in Gulf states residents.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 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
- Sub-Chronic Microcystin-LR Liver Toxicity in Preexisting Diet-Induced Nonalcoholic Steatohepatitis in Rats.Toxins · 2019Article
- Vinyl chloride-induced interaction of nonalcoholic and toxicant-associated steatohepatitis: Protection by the ALDH2 activator Alda-1.Redox biology · 2019Article
- Interaction of volatile organic compounds and underlying liver disease: a new paradigm for risk.Biological chemistry · 2018Review
- Exposure to Vinyl Chloride and Its Influence on Western Diet-Induced Cardiac Remodeling.Chemical research in toxicology · 2018Article
- Effects of Rhizoma Alismatis extract on biochemical indices and adipose gene expression in oleic acid-induced hepatocyte injury in Jian carp (Cyprinus carpio var. Jian).Fish physiology and biochemistry · 2018Article
- Vinyl chloride dysregulates metabolic homeostasis and enhances diet-induced liver injury in mice.Hepatology communications · 2018Article
- Exposure to sub-parts per million levels of vinyl chloride can increase the risk of developing liver injury.Hepatology communications · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundVinyl chloride (VC) causes toxicant-associated steatohepatitis at high exposure levels. Recent work by this group suggests that underlying liver disease may predispose the liver to VC hepatotoxicity at lower exposure levels. The most common form of underlying liver disease in the developed world is non-alcoholic fatty liver disease (NAFLD). It is well-known that the type of dietary fat can play an important role in the pathogenesis of NAFLD. However, whether the combination of dietary fat and VC/metabolites promotes liver injury has not been studied.
methodsMice were administered chloroethanol (CE - a VC metabolite) or vehicle once, 10weeks after being fed diets rich in saturated fatty acids (HSFA), rich in poly-unsaturated fatty acids (HPUFA), or the respective low-fat control diets (LSFA; LPUFA).
resultsIn control mice, chloroethanol caused no detectable liver injury, as determined by plasma transaminases and histologic indices of damage. In HSFA-fed mice, chloroethanol increased HSFA-induced liver damage, steatosis, infiltrating inflammatory cells, hepatic expression of proinflammatory cytokines, and markers of endoplasmic reticulum (ER) stress. Moreover, markers of inflammasome activation were increased, while markers of inflammasome inhibition were downregulated. In mice fed HPUFA all of these effects were significantly attenuated.
conclusionsChloroethanol promotes inflammatory liver injury caused by dietary fatty acids. This effect is far more exacerbated with saturated fat, versus poly-unsaturated fat; and strongly correlates with a robust activation of the NLRP3 inflammasome in the saturated fed animals only. Taken together these data support the hypothesis that environmental toxicant exposure can exacerbate the severity of NAFLD/NASH.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.