Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Internet Explorer is no longer a supported browser.

This website may not display properly with Internet Explorer. For the best experience, please use a more recent browser such as the latest versions of Google Chrome, Microsoft Edge, and/or Mozilla Firefox. Thank you.

Your Environment. Your Health.

University of North Carolina-Chapel Hill: Dataset Details, ID=GSE24278

Superfund Research Program

Elucidating Risks: From Exposure and Mechanism to Outcome

Center Director: Rebecca C. Fry
Grant Number: P42ES005948
Funding Period: 1992-2018
View this project in the NIH Research Portfolio Online Reporting Tools (RePORT)

Learn More About the Grantee

Visit the grantee's eNewsletter page Visit the grantee's eNewsletter page Visit the grantee's Twitter page Visit the grantee's Video page

Title: The effect of trichloroethylene on gene expression in mouse liver

Accession Number: GSE24278

Link to Dataset: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE24278

Repository: Gene Expression Omnibus (GEO)

Data Type(s): Gene Expression

Experiment Type(s): Expression profiling by array

Organism(s): Mus musculus

Summary: Trichloroethylene (TCE) is a widely used industrial chemical, and a common environmental contaminant. It is a well-known carcinogen in rodents and a probable carcinogen in humans. Studies utilizing panels of mouse inbred strains afford a unique opportunity to understand both metabolic and genetic basis for differences in responses to TCE. We tested the hypothesis that individual and liver-specific toxic effects of TCE are genetically controlled and that the mechanisms of toxicity and susceptibility can be uncovered by exploring responses to TCE using a diverse panel of inbred mouse strains. TCE (2100 mg/kg) or corn oil vehicle were administered by gavage to 6-8 wk old male mice of 15 mouse strains. Serum and liver were collected at 2, 8, and 24 hr post dosing and were analyzed for TCE metabolites, hepatocellular injury and gene expression of liver. TCE metabolism, as evident from the levels of individual oxidative and conjugative metabolites, varied considerably between strains. TCE treatment-specific effect on the liver transcriptome was strongly dependent on the individual’s genetic background. PPAR-mediated molecular networks, consisting of the metabolism genes known to be induced by TCE, represent some of the most pronounced molecular effects of TCE treatment in mouse liver that are dependent on the individual’s genetic background. Conversely, cell death, liver necrosis, and immune mediated response pathways which are affected by TCE treatment in liver are largely genetic background-independent. These studies provide better understanding of the mechanisms of TCE-induced toxicity anchored on metabolism and genotype-phenotype correlations that may define susceptibility or resistance.

Publication(s) associated with this dataset:
  • Bradford BU, Lock EF, Kosyk O, Kim S, Uehara T, Harbourt D, DeSimone MC, Threadgill DW, Tryndyak VP, Pogribny IP, Bleyle L, Koop DR, Rusyn I. 2011. Interstrain differences in the liver effects of trichloroethylene in a multistrain panel of inbred mice. Toxicol Sci 120(1):206-217. doi:10.1093/toxsci/kfq362 PMID:21135412 PMCID:PMC3044200
Back
to Top