ABSTRACT
A good correlation between nitrate intake and gastric cancer mortality in various countries has been documented. 1 Nitrate taken from diet and secreted into saliva is converted into nitrite by bacteria in the oral cavity, 2 , 3 which may serve as an agent to produce carcinogenic compounds by reaction with their precursors under gastric conditions. Recently, nitrite and nitrate have been found to be produced from arginine in mammalian cells, and immuno-stimulants are known to enhance the synthesis of nitrite and nitrate. 4 Dialkylamines and trialkylamines are well-known precursors for the N-nitrosamines in foods. These amines are generally found in fish meats and they can undergo nitrosation by reaction with nitrite under gastric conditions to form carcinogenic dialkylnitrosamines. 5 , 6 Direct-acting genotoxic N-nitrosamidines and nitrosamides such as N-alkyl-N′-nitro-N-nitrosoguanidine and N-alkyl-A-nitrosourea have been known to induce cancer in the glandular stomach of experimental animals. 7 – 10 These types of direct-acting genotoxic compounds can be produced by reaction of their precursors if present in foods with nitrite under acidic conditions similar to those of gastric juice. Recent hypotheses for the development of gastric cancer suggest that exposure in the stomach to direct-acting genotoxic N-nitroso compounds, formed endogenously, may be involved. 11
