There are conflcting reports about selenium levels in prostate cancer. Rearch indicates that there are reduced levels of selenoprotein P in prostate cancer. High levels of selenoprotein P are also associcated with low risk of high grade prostate cancer. Other research indicates that circulating selenium levels are high in advanced prostate cancer.
I have been arguing that in many illnesses that the transsulfuration pathway is dysregulated. Besides synthesizing L-cysteine from homocysteine the transsulfuration pathway also metabolizes L-selenomethionine which is the food form of selenium. L-selenomethionine is stored in the body via replacing methionine in proteins. If selenium never makes it out of selenomethionine there could be both high selenium levels and low selenoprotein levels. High levels of circulating selenium in advanced prostate cancer could paradoxcially indicate that there are selenoprotein deficiencies in prostate cancer which appears to be the case both for selenoprotein P and glutathione peroxidase. Glutathione peroxidase, another selenoprotein, is also reduced in prostate cancer.
Se-methylselenocysteine is a form of selenium that is not metabolized via the transsulfuration pathway so formation of selenoproteins from Se-methylselenocysteine would not be impeded by dysregulation of the transsulfuration pathyway. While supplemental selenomethionine apparently does not reduce the risk of prostate cancer supplemental Se-methylselenocysteine could reduce the risk of prostate cancer. The advantage of Se-methylselenocysteine as a cancer preventive could be exactly due to metabolism of Se-methylselenocysteine not depending on the transsulfuration pathway.