© 1992 Oxford University Press
research-article |
Chloroform inhibits the development of diethylnitrosamine-initiated, phenobarbital-promoted 
-glutamyltranspeptidase and placental form glutathione S-transferase-positive foci in rat liver
US Environmental Protection Agency, Environmental Monitoring Systems Laboratory 26 West Martin Luther King Drive, Cincinnati, OH 45268
1Pathology Associates Center Park Drive, West Chester, OH 45069, USA
In this study we demonstrate that chloroform, a widely used industrial solvent, a medicinal chemical and a common drinking water contaminant, reduces the number of detectable preneoplastic enzyme-altered foci [
-glutamyl-transpeptidase-positive (GGT+) and placental form glutathione S-transferase-positive (GST-P+)] in the liver of male Fischer 344 rats. The animals were given a partial hepatectomy and 18 h later received a single oral dose of either 0.5 mmol/kg diethymhrosamine (DENA) or saline. Two weeks later, groups of 12 animals were started on drinking water containing phenobarbital with varying concentrations (200–1800 mg/1) of chloroform for 12 weeks. Treated and control animals were killed and the number and the volume of GGT+ and GST-P+ expressing hepatic foci were tabulated. The numbers of foci per unit volume (and per unit area), the percent focal volume and the focal liver were reduced by chloroform in a dose-dependent manner. The mean focal volume was not influenced by chloroform. A plausible explanation for these results could be that chloroform exerts its focal inhibitory effect either by selectively killing the putative initiated cells, by retarding the inherent growth rate of enzyme-altered cells or by reducing the effectiveness of the promoter, phenobarbital. The available evidence suggests that the first hypothesis is the most likely explanation for these observations. These results are consistent with earner studies showing that chloroform inhibits tumorigenesis in rodents.