ENHANCEMENT OF BOP-INDUCED PANCREATIC CARCINOGENESIS IN SELENIUM-FED SYRIAN GOLDEN-HAMSTERS UNDER SPECIFIC DIETARY CONDITIONS
ENHANCEMENT OF BOP-INDUCED PANCREATIC CARCINOGENESIS IN SELENIUM-FED SYRIAN GOLDEN-HAMSTERS UNDER SPECIFIC DIETARY CONDITIONS
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DOI：
10.1080/01635588809513966
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发表时间：
1988-01-01
影响因子：
2.9
通讯作者：
POUR, PM
中科院分区：
文献类型：
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作者：
BIRT, DF;JULIUS, AD;POUR, PM
本实验研究了日粮中添加硒(Se)对Byn-亚硝基(2-氧丙基)胺(BOP)诱发叙利亚金黄地鼠胰腺癌的影响。饲喂六种不同组合的试验性日粮：0.1、2.5、5.0ppmSe来自亚硫酸钠，2.5ppm来自D，L-硒蛋氨酸，在低(6.0%)或高(24.4%)脂肪日粮中。Se治疗在BOP治疗前四周开始，高脂饮食从最后一次BOP治疗后一周开始喂养。没有观察到Se抑制胰腺癌的证据；事实上，在某些实验条件下，高Se饮食增加了胰腺癌的产量。然而，促进生长所需的饮食条件在性别之间有所不同。接受含Se 2.5ppm的高脂肪饮食的雄性仓鼠比接受0.1ppm Se水平的雄性仓鼠患癌症更多。在这些饮食中，癌症发生率和死亡率没有差别。从D.L-硒蛋氨酸中摄取2.5ppm Se的女性患胰腺癌的几率高于那些摄入0.1ppm Se的女性。然而，在喂食这些食物的雄性仓鼠中，癌症的产率并没有差异。考虑到高硒饮食，尤其是当比较高脂肪饮食中的硒水平时，金黄地鼠的腺泡细胞结节产量通常会减少。预先给予0.1或2.5ppm的Se不影响胰腺DNA从导管细胞中的洗脱常数，表明Se对BOP诱导的这些细胞DNA单链断裂的修复没有影响。在腺泡细胞中的测量表明，喂食2.5ppm硒的仓鼠比喂食0.1ppm硒的仓鼠单链断裂修复更快。
We measured the effects of dietary selenium (Se) on pancreatic cancer induced in Syrian golden hamsters byN‐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.