Institut für Rechtsmedizin, Ludwig-Maximillians Universität, Munich, Germany.
Biol Trace Elem Res. 2010 May;134(2):180-7. doi: 10.1007/s12011-010-8636-y. Epub 2010 Feb 20.
Cadmium (Cd) from cigarette smoke, environmental, and nutritional sources accumulates in the human prostate where it interacts with selenium (Se) in a manner suggesting the formation of a 1:1 Cd-Se-protein complex. At low Cd exposures and adequate Se status, this interaction may be beneficial as it results in the detoxification of Cd. At higher exposures, Cd may weaken or abolish the anticarcinogenic effects of Se and increase prostate cancer risk. In some older men and especially in smokers, Cd levels in prostates reach levels in stoichiometric excess over Se, which may be the reason why heavy smokers are at higher risk of developing lethal forms of prostate cancer. In the liver and the kidneys, Cd accumulates as well, but in these organs, Cd is efficiently sequestered through metallothionein formation. In the prostate, this mode of detoxification is not available or less efficient, causing Cd to interact with Se and to increase prostate cancer risk.
来自香烟烟雾、环境和营养来源的镉 (Cd) 在人类前列腺中积累,与硒 (Se) 以一种暗示形成 1:1 Cd-Se-蛋白质复合物的方式相互作用。在低镉暴露和足够的硒状态下,这种相互作用可能是有益的,因为它导致了镉的解毒。在更高的暴露下,镉可能会削弱或消除硒的抗癌作用,并增加前列腺癌的风险。在一些老年男性中,尤其是在吸烟者中,前列腺中的镉水平达到了与硒的化学计量过剩的水平,这可能就是为什么重度吸烟者患致命性前列腺癌的风险更高的原因。在肝脏和肾脏中,镉也会积累,但在这些器官中,镉通过形成金属硫蛋白被有效地隔离。在前列腺中,这种解毒模式不可用或效率较低,导致镉与硒相互作用并增加前列腺癌的风险。