To evaluate the role of high-dose dietary zinc in the process of prostate malignancy,60 Sprague-Dawley rats were randomly divided into four groups:tumor induction with carcinogen and hormone (group 1),oral zinc adm...To evaluate the role of high-dose dietary zinc in the process of prostate malignancy,60 Sprague-Dawley rats were randomly divided into four groups:tumor induction with carcinogen and hormone (group 1),oral zinc administration without tumor induction (group 2),oral zinc administration with tumor induction (group 3) and a control without zinc administration or tumor induction (group 4). Zinc was supplied orally in the form of zinc sulfate heptahydrate dissolved in drinking water to groups 2 and 3 for 20 weeks. Although the serum level of zinc measured at 20 weeks was maintained similarly in each group (P = 0.082),intraprostatic zinc concentrations were statistically different. Group 1 prostates contained the least amount of zinc in both the dorsolateral and ventral lobes at levels of 36.3 and 4.8 μg g^-1,respectively. However,in group 3,zinc levels increased in both lobes to 59.3 and 12.1 μg g^-1,respectively,comparable with that of group 4 (54.5±14.6 and 14.1±2.4 μg g^-1). In spite of these increases in zinc concentration,the prevalence of prostate intraepithelial neoplasm was rather increased in group 3 (53.3% and 46.7%) compared with group 1 (33.3% and 33.3%) in both dorsolateral and ventral prostate lobes. Although prostate intraepithelial neoplasm did not develop in any prostate in group 4,zinc administration did induce prostate intraepithelial neoplasm in group 2 (46.7% and 40.0%). Thus,although high dietary zinc increased intraprostatic zinc concentrations,it promoted,instead of preventing,prostate intraepithelial neoplasm in a murine prostate malignancy induction model.展开更多
文摘To evaluate the role of high-dose dietary zinc in the process of prostate malignancy,60 Sprague-Dawley rats were randomly divided into four groups:tumor induction with carcinogen and hormone (group 1),oral zinc administration without tumor induction (group 2),oral zinc administration with tumor induction (group 3) and a control without zinc administration or tumor induction (group 4). Zinc was supplied orally in the form of zinc sulfate heptahydrate dissolved in drinking water to groups 2 and 3 for 20 weeks. Although the serum level of zinc measured at 20 weeks was maintained similarly in each group (P = 0.082),intraprostatic zinc concentrations were statistically different. Group 1 prostates contained the least amount of zinc in both the dorsolateral and ventral lobes at levels of 36.3 and 4.8 μg g^-1,respectively. However,in group 3,zinc levels increased in both lobes to 59.3 and 12.1 μg g^-1,respectively,comparable with that of group 4 (54.5±14.6 and 14.1±2.4 μg g^-1). In spite of these increases in zinc concentration,the prevalence of prostate intraepithelial neoplasm was rather increased in group 3 (53.3% and 46.7%) compared with group 1 (33.3% and 33.3%) in both dorsolateral and ventral prostate lobes. Although prostate intraepithelial neoplasm did not develop in any prostate in group 4,zinc administration did induce prostate intraepithelial neoplasm in group 2 (46.7% and 40.0%). Thus,although high dietary zinc increased intraprostatic zinc concentrations,it promoted,instead of preventing,prostate intraepithelial neoplasm in a murine prostate malignancy induction model.