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In a series of extensive studies on gastric carcinogenesis, we have used Sprague-Dawley rats to examine the morphologic, histochemical, and biochemical effects of risk and protective factors on N-methyl-N'-nitro-N-nitroso guanidine (MNNG)-induced tumors in an attempt to link early observations with the end-point lesion, gastric cancer. We have observed that the putative risk factors sodium chloride (NaCl); a mixture of bile acids; aspirin; alcohol; and nitrite enhance MNNG-induced neoplasia of the gastric mucosa. On the other hand butylated hydroxyanisol (BHA), Se and difluromethylornithine (DFMO) were protective and inhibited the induction of gastric mucosal neoplasia. In most cases, early changes detected by a number of criteria correlated with the end-point, gastric neoplasia. This model appears to be useful in screening and evaluating chemicals for risk for or protection against gastric cancer.
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Newberne et al. (1987) studied this question.
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