Methylselenocysteine and Methylseleninic acid
Feb 20 2016
Monomethylated selenium forms that are precursors of methylselenol, such as methylseleninic acid, differ in metabolism and anticancer activities in preclinical cell and animal models from seleno-methionine that had failed to exert preventive efficacy against prostate cancer in North American men.
Cancer Med. 2014 Feb 7. Methylseleninic acid elevates REDD1 and inhibits prostate cancer cell growth despite AKT activation and mTOR dysregulation in hypoxia.Sinha I, Allen JE, Pinto JT, Sinha R.Author informationAbstractMethylseleninic acid (MSeA) is a monomethylated selenium metabolite theoretically derived from subsequent β-lyase or transamination reactions of dietary Se-methylselenocysteine that has potent antitumor activity by inhibiting cell proliferation of several cancers. Our previous studies showed that MSeA promotes apoptosis in invasive prostate cancer cells in part by downregulating hypoxia-inducible factor HIF-1α. We have now extended these studies to evaluate the impact of MSeA on REDD1 (an mTOR inhibitor) in inducing cell death of invasive prostate cancer cells in hypoxia. In both PTEN+ and PTEN- prostate cancer cells we show that MSeA elevates REDD1 and phosphorylation of AKT along with p70S6K in hypoxia. Furthermore, REDD1 induction by MSeA is independent of AKT and the mTOR inhibition in prostate cancer cells causes partial resistance to MSeA-induced growth reduction in hypoxia. Our data suggest that MSeA induces REDD1 and inhibits prostate cancer cell growth in hypoxia despite activation of AKT and dysregulation of mTOR.
Anal Chim Acta. 2009;
Speciation of selenium dietary supplements; formation of S-methylselenocysteine and other selenium compounds.
Department of Chemistry, University of Massachusetts
Speciation of selenium is of interest because it is both essential and toxic to humans, depending on the species and the amount ingested. Following indications that selenium supplementation could reduce the incidence of some cancers, selenium-enriched yeast and other materials have been commercialized as supplements. Most dramatically however, the SELECT trial that utilized l-selenomethionine as the active supplement was terminated in 2008 and there is much debate regarding both the planning and the results of efficacy studies. Further, since dietary supplements are not regulated as pharmaceuticals, there are concerns about the quality, storage conditions, stability and selenium content in selenium supplements. Enzymatic hydrolysis enabled selenium speciation profiles to be obtained by high performance liquid chromatography with inductively coupled plasma mass spectrometry (HPLC-ICP-MS) and following derivatization gas chromatography with atomic emission detection (GC-AED). Coated fiber solid phase microextraction (SPME) was used to extract volatile selenium species for determination by GC-AED and GC-MS. Similar speciation patterns were observed between yeast-based supplements subject to extended storage and those heated briefly at elevated temperatures. All the yeast-based supplements and one yeast-free supplement formed S-(methylseleno)cysteine on heating. Evidence was obtained in support of the hypotheses that S-(methylseleno)cysteine is formed from a reaction between dimethyldiselenide and cysteine or cystine.
I would appreciate it if you could address the benefits of methylselenocysteine in one of his future newsletters. I see this supplement is being offered by other companies. The positive effects on reducing cancer risk and boosting the immune system are things I'd like to see you comment on.