EFFECTS OF 4-(METHYLNITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE (NNK) ON N-NITROSOBIS(2-OXOPROPYL)AMINE (BOP)-INITIATED CARCINOGENESIS IN HAMSTERS

The effects of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) ad ministration during the post-initiation phase of carcinogenesis were i nvestigated in hamsters treated with N-nitrosobis(2-oxopropyl)amine (B OP). Female Syrian golden hamsters were given a single s.c. injection of BOP at a dose of 10 mg/kg and then administered 3 ppm (H) or 1 ppm (L) NNK in their drinking water for the following 87 weeks. Additional groups of animals received the BOP injection alone, or only the 3 or 1 ppm NNK treatments as BOP-negative controls. At week 88 of the exper iment, all surviving animals were sacrificed and development of prolif erative lesions was assessed histopathologically. The results showed n o statistically significant influence on pancreatic adenocarcinomas or dysplastic lesions, although the incidence and the number of atypical hyperplasias in the pancreas head in the BOP/NNK (L) group was signif icantly increased as compared to BOP alone group values (P < 0.05). Si milarly, the NNK treatments did not affect the incidences or multiplic ities of neoplastic or hyperplastic lesions in the endocrine pancreas, lung, liver or kidney. Thus, the present experiment demonstrates that the tobacco-specific carcinogen NNK does not enhance BOP-induced hams ter tumorigenesis when given in the promotion phase.