Abstract
(1) The in vivo reduction of nitrate occurred in the absence of a gastrointestinal flora in the rat and nitrate reductase activity was found in the mucosae of the stomach and small intestine. (2) The pH of the intestinal tract was decreased by the gut flora but its influence on stomach pH was less clear. Fasting increased the pH of the gastrointestinal tract in CV rats but had little effect in GF rats. (3) N-nitrosation occurred primarily in the acid environment of the stomach and in rats fed a commercial diet, was potentiated by unidentified products of microbial metabolism. In rats fed a purified diet, no influence of the flora was observed. (4) The endogenous synthesis of nitrate was demonstrated and an increase in the protein content of the diet increased both nitrate and nitrosamine synthesis. The gastrointestinal flora appeared to reduce some of the endogenously formed nitrate and it is proposed that the synthesis of nitrate occurred from nitrogenous end products of protein catabolism. (5) The inhibition of N-nitrosation by dietary fats was demonstrated, butterfat having the greatest inhibitory effect. The effect of butterfat was shown to be primarily the result of the inhibition of nitrate reductase activity in the stomach. (6) The protein and fat content of the diet and the presence of a microbial flora had no effect on nitrosamine N-demethylating activity by liver S_9 fractions and a higher activity was present in fractions from male rats. Nitrosamine N-demethylating activity was also present in small intestinal S_9 fractions and a protective influence of the small intestinal mucosa in nitrosamine-induced damage is proposed.