Chlorinated aliphatic hydrocarbons promote lipid peroxidation in vascular cells.

Chlorinated aliphatic hydrocarbons such as trichloroethylene and trichloroethane cause acute and chronic cardiotoxicities via mechanisms that are still obscure. Some of these toxic effects may result from free-radical-induced membrane damage to the vascular tissues. The pro-oxidant effects of carbon tetrachloride, trichloroethylene, 1,1,1-trichloroethane, 1,2-dichloroethane, and trans-1,2-dichloroethylene were assessed in cultured arterial endothelial and aortic smooth muscle cells. Exposure of the cells to the above chemicals alone did not increase the formation of thiobarbiturate reactive products above background levels. However, in the presence of low levels of iron (3.1-25 microM Fe3+ chelated by ADP), all five agents promoted lipid peroxidation up to 200% of control. The rank order of potency is carbon tetrachloride greater than or equal to trichloroethylene greater than 1,1,1-trichloroethane greater than trans-1,2-dichloroethylene greater than 1,2-dichloroethane. The synergistic interaction between iron and chlorinated hydrocarbons in promoting lipid peroxidation may contribute to the cardiotoxicities of these agents.