ArticleToxicology and applied pharmacology2013
Metabolic changes and DNA hypomethylation in cerebellum are associated with behavioral alterations in mice exposed to trichloroethylene postnatally.
Article in Toxicology and applied pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- The industrial solvent trichloroethylene induces LRRK2 kinase activity and dopaminergic neurodegeneration in a rat model of Parkinson's disease.Neurobiology of disease · 2021Article
- Effect of environmental toxicants on neuronal functions.Environmental science and pollution research international · 2020Review
- Complex epigenetic patterns in cerebellum generated after developmental exposure to trichloroethylene and/or high fat diet in autoimmune-prone mice.Environmental science. Processes & impacts · 2020Article
- Trichloroethylene exposure in mid-pregnancy decreased fetal weight and increased placental markers of oxidative stress in rats.Reproductive toxicology (Elmsford, N.Y.) · 2019Article
- Clinical and Molecular Characteristics of Mitochondrial Dysfunction in Autism Spectrum Disorder.Molecular diagnosis & therapy · 2018Review
- Assessment of the Endocrine-Disrupting Effects of Trichloroethylene and Its Metabolites Using in Vitro and in Silico Approaches.Environmental science & technology · 2018Article
- Toxic Effects of Trichloroethylene on Rat Neuroprogenitor Cells.Frontiers in pharmacology · 2018Article
- A single dose of trichloroethylene given during development does not substantially alter markers of neuroinflammation in brains of adult mice.Journal of immunotoxicology · 2017Article
- Oxidative Stress Challenge Uncovers Trichloroacetaldehyde Hydrate-Induced Mitoplasticity in Autistic and Control Lymphoblastoid Cell Lines.Scientific reports · 2017Article
- Inflammatory and oxidative stress-related effects associated with neurotoxicity are maintained after exclusively prenatal trichloroethylene exposure.Neurotoxicology · 2017Article
- A framework and case studies for evaluation of enzyme ontogeny in children's health risk evaluation.Journal of toxicology and environmental health. Part A · 2017Article
- Epigenetic Toxicity of Trichloroethylene: A Single-Molecule Perspective.Toxicology research · 2016Article
- Alcohol Withdrawal and Cerebellar Mitochondria.Cerebellum (London, England) · 2015Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Previous studies demonstrated that low-level postnatal and early life exposure to the environmental contaminant, trichloroethylene (TCE), in the drinking water of MRL+/+ mice altered glutathione redox homeostasis and increased biomarkers of oxidative stress indicating a more oxidized state. Plasma metabolites along the interrelated transmethylation pathway were also altered indicating impaired methylation capacity. Here we extend these findings to further characterize the impact of TCE exposure in mice exposed to water only or two doses of TCE in the drinking water (0, 2, and 28mg/kg/day) postnatally from birth until 6weeks of age on redox homeostasis and biomarkers of oxidative stress in the cerebellum. In addition, pathway intermediates involved in methyl metabolism and global DNA methylation patterns were examined in cerebellar tissue. Because the cerebellum is functionally important for coordinating motor activity, including exploratory and social approach behaviors, these parameters were evaluated in the present study. Mice exposed to 28mg/kg/day TCE exhibited increased locomotor activity over time as compared with control mice. In the novel object exploration test, these mice were more likely to enter the zone with the novel object as compared to control mice. Similar results were obtained in a second test when an unfamiliar mouse was introduced into the testing arena. The results show for the first time that postnatal exposure to TCE causes key metabolic changes in the cerebellum that may contribute to global DNA methylation deficits and behavioral alterations in TCE-exposed mice.
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