Ethanol-Induced Changes in Trichloroethene Toxicity
Abstract
This project was to determine the extent to which metabolism of trichloroethylene (TCE) to trichloroacetic acid (TCA) was responsible for its hepatotoxic and hepatocarcinogenic effects in rodents. Ethanol was used as a more or less selective means of decreasing the production of TCA. This information was useful in determining whether these effects are relevant to human exposures to these chemicals. During the first year of this project, it was established that dichloroacetic acid (DCA), trichloroacetic acid and chloral hydrate (CH) all are capable of inducing single strand breaks in hepatic DNA of both mice and rats in vivo at much lower doses that could TCE. Metabolism studies suggest that the production of TCA can be modified by ethanol coadministration. Experiments revealed that DCA produces a cytomegally that is seen uniformly throughout the liver of the mouse. This effect is characterized by massive accumulations of glycogen. It does not produce this effect in rats given even higher doses, nor is the effect duplicated completely by TCA. In addition, mice treated with DCA are displaying focal areas of change that appear preneoplastic after only 24 weeks of treatment with DCA. These results suggest that DCA may play a more important role in the hepatotoxic and hepatocarcinogenic effects of TCE than had been previously appreciated. Keywords: Trichloroethylene, Hepatotoxicity, Ethanol, Hepatocarcinogenicity.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 14, 1987
- Accession Number
- ADA187322
Entities
People
- Richard J. Bull
Organizations
- Washington State University