Chlorinated Hydrocarbon Toxicity

Abstract

In mice, an 18-hour pretreatment with acetone or isopropyl alcohol enhanced the capacity of threshold doses of chloro form, 1,1,2-trichloroethane, and trichloroethylene to produce an increased hepatotoxic response as measured by increases in serum glutamic pyruvic transaminase activity. The most marked potentiation was seen with chloroform. The hepatotoxicity of 1,1,1-trichloroethane was not augmented by prior administration of isopropyl alcohol or acetone. The ability of isopropyl alcohol or acetone to potentiate the hepatotoxic response of these agents is proportional to the basic hepatotoxicity of the agent involved.