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The influence of dietary thiocyanate (SCN-) on N-nitrosation in vivo was investigated over 14 min following the administration, by stomach tube, of single doses of sodium nitrite and dimethylamine hydrochloride to male albino Wistar rats whose diet contained appreciable quantities of bound cyanide (cyanogenic glycosides) and free (nonglycosidic) cyanide. The rate of disappearance of the nitrosating agent (NO2-) from the stomach in control animals showed a high linear correlation (r = -0.84) with gastric N-nitrosation, as measured by metabolism (N-demethylation) of 'formed' nitrosamine in liver tissue isolated from these animals. This statistical relationship was significantly increased (r = 0.98), as well as the rate of NO2- utilization and the activity of the N-demethylase enzyme, in animals fed the test diet. Stomach SCN- content was well correlated with both stomach NO2- concentration (r = -0.95) and liver N-demethylase activity (r = +0.93). Interactions, in vivo, between thiocyanate ion and nitrosamine precursors ingested in food may enhance nitrosamine carcinogenesis.
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Maduagwu et al. (1988) studied this question.
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