Enhancement of BOP‐induced pancreatic carcinogenesis in selenium‐fed Syrian Golden hamsters under specific dietary conditions

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Abstract
We measured the effects of dietary selenium (Se) on pancreatic cancer induced in Syrian golden hamsters by N‐nitrosobis(2‐oxopropyl)amine (BOP). The animals were fed six experimental diets that contained different combinations of the following: 0.1, 2.5, or 5.0 ppm Se from sodium selenite or 2.5 ppm Se from D,L‐selenomethionine in either a low (6.0 %)‐or high (24.4%)‐fat diet. Se treatment was begun four weeks before BOP treatment, and the high‐fat diet was fed from one week after the last BOP treatment. No evidence for inhibition of pancreatic cancer by Se was observed; in fact, with some experimental conditions, high‐Se diets increased the pancreatic carcinoma yield. However, the dietary conditions needed for enhancement differed between the sexes. The male hamsters that received the high‐fat diet containing 2.5 ppm Se had more carcinomas than did males given the 0.1 ppm Se level. Carcinoma yields infernales did not differ between these diets. Females that received 2.5 ppm Se from D.L‐selenomethionine had a greater pancreatic carcinoma yield than did those given 0.1 ppm Se diet. However, carcinoma yields did not differ in males fed these diets. Acinar cell nodule yields were generally reduced in hamsters given the high‐Se diets, especially when Se levels in the high‐fat diets were compared. Prefeeding 0.1 or 2.5 ppm Se did not influence the elution constants of pancreatic DNA from ductal cells, indicating no effect of Se on the repair of BOP‐induced, single‐strand breaks in DNA from these cells. Measurements in acinar cells suggested a more rapid repair of single‐strand breaks in hamsters prefed 2.5 ppm Se than in those prefed 0.1 ppm Se.