The Effects of Diethyldithiocarbamate on the Metabolism and Hepatotoxicity of Trichloroethylene.
- Author:
Byung Sun CHOI
1
;
Jung Duck PARK
;
Yeon Pyo HONG
Author Information
1. Department of Preventive Medicine and Community Health, College of medicine, Chung-Ang University, Korea. bschoi@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Trichloroethylene;
Cytochrome P450 2E1;
Diethyldithiocarbamate;
Metabolism;
Protective agents
- MeSH:
Animals;
Body Weight;
Cytochrome P-450 CYP2E1;
Ditiocarb*;
Liver;
Metabolism*;
Necrosis;
Protective Agents;
Rats;
Trichloroacetic Acid;
Trichloroethylene*
- From:Korean Journal of Occupational and Environmental Medicine
2002;14(3):257-269
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: The purpose of this study was to evaluate the trichloroethylene (TCE) metabolism, acute toxicity, and the effects of diethyldithiocarbamate (DDTC) on the acute toxicity in TCE-intoxicated rats. METHODS: TCE was administered orally at doses of 600, 1,200 and 2,400 mg/kg of body weight following pretreatment with either saline or 500 mg/kg of DDTC. 12 hours after administration of TCE, the concentrations of TCE, trichloroacetic acid (TCA) and trichloroethanol (TCEOH) in the blood and solid organs, and the histopathological changes in each organ were examined. RESULTS: The level of CYP2E1 markedly decreased in the DDTC-pretreated groups. The CYP2E1 content in the TCE-treated rats increased in a dose-dependent manner. The concentrations of TCE and TCEOH were highest in the liver, and the level of TCA was highest in the blood. The DDTC-pretreated rats had a markedly increased level of TCE and decreased levels of TCA and TCEOH, than the rats pretreated with saline. These findings indicated that CYP2E1 was important in the metabolism of TCE. From the histopathological findings, centrilobular necrosis was observed in the livers of the TCE-treated rats, but no significant change was found in those rats pretreated with DDTC. CONCLUSIONS: DDTC is considered to be effective in protecting TCE-induced hepatic damage because it inhibits the TCE metabolism.
