RESUMEN
The biotransformation of trichloroethylene (TCY) was studied in male Sprague-Dawley rats and in human hepatocyte suspensions to aid in estimating the potential for hepatocarcinogenesis in humans. The major metabolites were qualitatively identical in both species, but rat hepatocytes metabolized about four times more TCY than did human hepatocytes under the same experimental conditions. The quantities of chloral hydrate, trichloroethanol (free plus conjugated) and trichloroacetic acid (TCA) were 15, 5 and 20 times greater, respectively, in rat hepatocyte suspensions. Since the TCA metabolite has been implicated in TCY-induced peroxisomal proliferation and hepatocarcinogenesis and rats form less TCA than do mice, which are susceptible to these effects, the results suggest that humans are at low risk from TCY exposure.