El-Bayoumy Karam, Richie John P, Boyiri Telih, Komninou Despina, Prokopczyk Bogdan, Trushin Neil, Kleinman Wayne, Cox Julie, Pittman Brian, Colosimo Steven
American Health Foundation, Valhalla, New York 10595, USA.
Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1459-65.
The mechanisms responsible for the protective role of selenium against the development of prostate cancer remain to be determined (L. C. Clark et al., J. Am. Med. Assoc., 276: 1957-1963, 1996). In the present study, we tested the hypothesis that selenium supplementation reduces oxidative stress. A secondary aim was to determine whether selenium-induced changes in testosterone (T) metabolism may also be involved. To this end, we conducted a double-blind, randomized, placebo-controlled trial of 247 micro g selenium/day administered p.o. in the form of Se-enriched yeast. Study subjects were 36 healthy adult males, 11 blacks and 25 whites, 19-43 years of age. Supplementation occurred over the first 9 months, after which all subjects were placed on placebo for an additional 3 months. Blood and urine were collected at baseline and after 3, 9, and 12 months. In the selenium group, plasma selenium levels were 2-fold higher than baseline values after 3 and 9 months and returned to 136% of baseline after 12 months (P < 0.0001), whereas in the placebo group, levels were unchanged. A 32% increase in blood glutathione (GSH) levels was observed after 9 months in the selenium group only (P < 0.05). This change coincided with a 26% decrease in protein-bound GSH (bGSH) and a 44% decrease in bGSH:GSH ratios (P < 0.05). The changes in GSH and bGSH were highly correlated with changes in plasma selenium concentrations and may reflect a decrease in oxidative stress. No changes were observed in either group for plasma T, dihydrotestosterone (DHT) or DHT:T ratios, suggesting that selenium had no effect on the alpha-reductase involved in the conversion of T to DHT. A small but significant decrease in prostate-specific antigen levels was observed after 3 and 9 months (P < 0.001), and this difference disappeared after 12 months. Future trials will test the above hypothesis in prostate cancer patients and in subjects at high risk for prostate cancer.
硒对前列腺癌发展具有保护作用的机制尚待确定（L.C.克拉克等人，《美国医学会杂志》，276: 1957 - 1963, 1996）。在本研究中，我们检验了补充硒可降低氧化应激这一假设。第二个目的是确定硒诱导的睾酮（T）代谢变化是否也与之有关。为此，我们进行了一项双盲、随机、安慰剂对照试验，口服以富硒酵母形式提供的每日247微克硒。研究对象为36名健康成年男性，11名黑人，25名白人，年龄在19至43岁之间。补充硒的过程持续前9个月，之后所有受试者再服用3个月安慰剂。在基线以及3、9和12个月后采集血液和尿液样本。在硒组中，3个月和9个月后血浆硒水平比基线值高出2倍，12个月后恢复至基线的136%（P < 0.0001），而在安慰剂组中，水平未发生变化。仅在硒组中，9个月后血液中谷胱甘肽（GSH）水平升高了32%（P < 0.05）。这一变化与蛋白结合型谷胱甘肽（bGSH）降低26%以及bGSH:GSH比值降低44%同时出现（P < 0.05）。GSH和bGSH的变化与血浆硒浓度变化高度相关，可能反映了氧化应激的降低。两组中血浆T、双氢睾酮（DHT）或DHT:T比值均未观察到变化，表明硒对参与T转化为DHT的α - 还原酶没有影响。在3个月和9个月后观察到前列腺特异性抗原水平有小幅但显著的下降（P < 0.001），12个月后这种差异消失。未来的试验将在前列腺癌患者和前列腺癌高危人群中检验上述假设。
