Hepatic Lesions in Mice after Continuous Inhalation Exposure to 1,1,1-Trichloroethane.

摘要

Male CF-1 mice (24-34 gm.) were exposed to either 250 ppm or 1000 ppm of 1,1,1-trichloroethane in air continuously for 14 weeks; control mice were exposed to room air. Serial sacrifice of exposed and control mice demonstrated significant changes in the centrilobular hepatocytes of animals in the 1000 ppm group. Moderate liver triglyceride accumulation was evident in the 1000 ppm group and peaked at 40 mg. per gm. of tissue (wet weight) after 7 weeks of exposure. Partical recovery was indicated by a decrease in the hepatic triglyceride level to 16 mg. per gm. by 14 weeks of exposure to 1000 ppm. Electron microscopic evaluation revealed that cytoplasmic alterations were most severe in centrilobular hepatocytes in the 1000 ppm group and were mild to minimal in the 250 ppm group. These alterations consisted of vesiculation of the rough endoplasmic reticulum, with loss of attached polyribosomes, increased smooth endoplasmic reticulum, microbodies, and triglyceride droplets. Necrosis of individual hepatocytes occurred in 40 % of the mice exposed to 1000 ppm for 12 weeks. Comparison of these findings to results obtained by other investigators studying dichloromethane indicates that these pathologic alterations were similar to those observed with dichloromethane, except for different time courses of the effects and different degrees of recovery. The toxic effects of 1,1,1-trichloroethane were similar to but less severe than those produced by carbon tetrachloride.