Toxicologic Evaluation of Trichloroacetic Acid: Effects on Rat Liver Peroxisomes and Enzyme Altered Foci.
Abstract
Trichloroacetic acid (TCA) is one of the major nonvolatile halogenated by-products formed during the process of water chlorination. Recent studies have indicated that TCA may be an effective stimulant of hepatic peroxisomal activity in the rat and mouse. It has been further suggested that TCA, a metabolite of trichloroethylene, may be involved in the hepatic carcinogenic effect of trichloroethylene. This research was designed to determine the relative potential of low-levels of TCA to produce toxic effects, including carcinogenicity, in an animal model. The initiating and promoting effects of TCA were investigated using a rat hepatic enzyme-altered foci (EAF) bioassay. No evidence was found to support any significant genotoxic or initiating activity by TCA. However, a significant induction of EAF in the promotion protocol was seen following TCA exposure. The ability of TCA to stimulate peroxisomal-dependent palmitoyl-CoA oxidation was also investigated. Only the high dose (5000 ppm) in the drinking water resulted in a significant, though minor, stimulation of peroxisomal enzyme activity. A single high dose (1500 mg/kg) of TCA did stimulate a large increase in hepatic ornithine decarboxylase activity when measured at 5 and 18 hours post exposure. No significant changes in hepatic mixed function oxidase activity was seen following TCA administration. No consistent or significant pathologic lesions could be attributed to TCA exposure at any phase of these studies.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 1986
- Accession Number
- ADA166379
Entities
People
- Michael J. Parnell
Organizations
- Air Force Institute of Technology