Oral bacteria can reduce nitrate to nitrite which, under the acidic conditions of the stomach, can react with amines in foods to form carcinogenic N-nitrosamines. In addition to dietary sources, a significant amount of nitrate is formed endogen-ously by the metabolism of nitric oxide—1mg/kg body weight/day (about the same as the average dietary intake), increasing 20-fold in response to inflammation and immune stimulation, and nitrate is secreted in saliva.
Ascorbate reacts with nitrite forming NO, NO2, and N2, so preventing the formation of nitrosa-mines. In addition to ascorbate in foods, there is considerable secretion of ascorbate in the gastric juice, and inhibition of gastric secretion for treatment of gastric ulcers, as well as reducing vitamin B12 absorption, also inhibits this presumably protective gastric secretion of ascorbate.
However, while ascorbate can deplete nitrosating compounds under anaerobic conditions, the situation may be reversed in the presence of oxygen. Nitric oxide reacts with oxygen to form N2O3 and N2O4, both of which are nitrosating reagents, and can also react with ascorbate to form NO and monodehydroascorbate. It is thus possible for ascor-bate to be depleted, with no significant effect on the total concentration of nitrosating species. It remains to be determined whether or not ascorbate has any significant effect in reducing the risk of nitrosamine formation and carcinogenesis.
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