The role of testosterone in the nasal cavity tumors induced by N-nitrosobis(2-oxopropyl)amine in rats.

In a previous study in rats we have shown that castration prior to weekly administration of N-nitrosobis(2-oxopropyl)amine (BOP) prevents induction of nasal and paranasal cavity (NPNC) tumors, indicating androgen dependency of these neoplasms. To investigate the possible inhibitory effect of testosterone withdrawal on the growth of NPNC tumors, in the present study rats were castrated following weekly treatment with BOP for 10, 20 or 30 weeks. This treatment did not alter the incidence, type, location, latency or multiplicity of NPNC tumors. However, simultaneous treatment of castrated rats with BOP and testosterone (T) yielded NPNC tumors in an incidence and patterns comparable to that seen in BOP-treated intact and BOP-plus-T-treated intact rats. Serological examination revealed abnormally high levels of T and 17-beta estradiol (E) in rats, which were killed immediately after 10, 20 or 30 weekly BOP administrations. The overall results suggest that the initiation but not the promotional stage of NPNC carcinogenesis is governed by androgens.

Interaction of dietary fat and protein on pancreatic carcinogenesis in Syrian golden hamsters.

The role of interactions between dietary fat and protein in experimental pancreatic cancer was determined in Syrian golden hamsters treated with N-nitrosobis(2-oxopropyl)amine (BOP). Two levels of corn oil [4.5 and 18 g/385 kilocalorie (kcal)] were fed with each of two levels of casein (9 g/385 kcal and 36 g/385 kcal), either before or after a single sc injection of BOP (10 mg/kg body wt) at 8 weeks of age. Control diet was fed at other times (9 g corn oil and 18 g casein/385 kcal). The pancreatic ductular carcinoma incidence and multiplicity (average No. of tumors/tumor-bearing animals) increased as dietary fat and protein levels rose in hamsters fed the four diets after carcinogen treatment. Enhanced carcinogenesis by high-fat (HF) diets occurred only in hamsters fed the high-protein (HP) level, and protein effects were seen only with the HF diets. The low-fat-low-protein (LF-LP) diet inhibited pancreatic carcinogenesis among the hamsters given the four diets before BOP treatment. Pancreatic adenoma yields were elevated in hamsters given either HF or HP diets following BOP treatment, by comparison with the low levels. However, when diets were fed before BOP treatment, an increased yield occurred with the rise in protein, but the yield was reduced in males with the increase in fat. Acinar cell nodules were observed primarily in hamsters fed LP levels after BOP, and their multiplicity was highest in those given the HF diet. The interaction between dietary fat and protein demonstrated the interdependence of the effects of these two nutrients on pancreatic carcinogenesis in hamsters.