Abstract
The effect of chronic administration of aminoacetonitrile (AAN) on the metabolism of 14C-diethylnitrosamine (DEN) was measured as a function of the ethylation of liver RNA and 14CO2 exhalation in rats continuously fed unlabeled carcinogen. The results were compared with those of acute experiments in which a single application of 14C-DEN led to 14CO2 exhalation and ethylation of liver RNA, whereas both effects were significantly lower after a single injection of AAN. After continuous feeding with DEN followed by a dose of BC-DEN, the exhalation of 14CO2 was reduced in those rats which had also been continuously treated with AAN. In rats fed DEN continuously but given no further treatment, no inhibition in the output of 14CO2 was recorded, compared with that of the acute experiment. However, the exhalation was prolonged. Chronic administration of AAN and DEN together also significantly decreased the ethylation rate of liver RNA in rats. The influence of AAN treatment during DEN carcinogenesis in rats was investigated. A change of organotropy with development of esophageal tumors was established. The possible function of carcinogen metabolism in induction of esophageal and liver tumors was discussed.