Induction of Cell Proliferation in the Forestomach of F344 Rats FoUowing Subchronic Administration of Styrene 7,8-0xide and Butylated Hydroxyanisole

for the 2% diet). to protein in vivo (20, 21). lt is possible, therefore, that SO and BHA were carcinogenic in the forestomach via a similar "nongenotoxic" mechanism of action, i.e., the stimulation 01' cell division induced by cytotoxicity and regenerative hyperplasia. This mechanism has been postulated for various forestomach carcinogens (22). BHA was demonstrated to have a strong hyperplasiogenic activity (17, 23), partieularly in the prefundic region 01' the forestomach, i.e., dose to the ridge forming the limit to the glandular stomach. This was also the region where BHA-induced squamous eell carcinomas were predominantly localized, a correspondence that might be of value 1'01' the analysis of the mechanism of carcinogenic action. In this study, SO was examined for an effect on cell proliferation kinetics in the forestomach. The activity 01' SO was compared to the one seen with the "nongenotoxic" forestomach carcinogen BHA, in order to investigate whether tumor induction by SO could be explained by a similar mechanism 01' action.