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[Dimethylamine].

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Animals↗

[Effect of human gastric juice on dimethylamine nitrosation by sodium nitrite].

The study was concerned with evaluation of the effect of human gastric juice (samples obtained from 157 subjects) on in vitro dimethylnitrosamine nitrosation by sodium nitrite versus gastric mucosa pathology (gastritis, polyps, ulcer, cancer), gastric juice pH and nitrate ion level. Also, the influence of gastric juice glycosaminoglycans and glycoproteins levels as well as N-acetylneuraminic acid isolated from porcine blood was assessed. An increased nitrosating activity of gastric juice was observed in cases of gastritis and ulcer and in those with low nitrate ion activity. Glycosaminoglycans and glycoproteins were found to inhibit nitrosation. N-acetylneuraminic acid in the concentrations used exerted no effect on dimethylnitrosamine nitrosation by sodium nitrite.

Dimethylamines↗

Effects of alkali and oxygen on nitrosation in dimethylamine-nitrite mixtures with and without reductants.

Two types of 'alkali effect', i.e., the formation of NDMA by alkylization of nitrite-DMA mixtures with and without reductants, were investigated. In the reductant-free system, the 'alkali effect' was found to increase with decreasing pH of the initial system. 'Cofactors' (some buffering agents or metallic ions) were essential for the 'alkali effect' in the presence of ascorbate, but were not necessary when tannic acid was the reductant. It may be concluded that free NO is released from nitrite by the action of reductants, with or without 'cofactors', and that N2O3 and/or N2O4, the nitrosating agents, are derived from NO via NO2 by air oxidation. Dinitrogen trioxide, generated from HNO2 in an acidic solution, and N2O4, derived from N2O3, are considered to be the main nitrosating agents producing the 'alkali effect' in the reductant-free system, but the presence of O2 also showed a remarkable enhancing effect on NDMA formation in this system.

Alkalies↗