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Best form of Selenium...L-Selenomethionine?


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#1 Magnus Greel

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Posted 02 March 2009 - 10:40 AM


I would like to add a selenium supplement to my regime, however having read some posts on this forum, I have seen studies reffering to risk of cancer, diabetes and also prostate cancer and wanted to hear what peoples thoughts are on the best form of selenium?
Whilst doing a search I came across a couple of studies which seem to suggest the selennomethonine form has some effect on inhibiting cancer growth?



Effects of selenomethionine on the gene expression profile of cloned human prostate cancer cells representing a phenotypic continuum of cancer progression.

Stewart J, Ware J, Boysen C, Gulati S, Zhou Z, Rosenfeld S, Kopelovich L, Kennedy AR.Department of Radiation Oncology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6072, USA.

We previously characterized three cell clones that were derived by limiting dilution from a human prostate cancer cell line (LNCaP) representing a phenotypic continuum of cancer progression (1). The present study was undertaken to examine the effects of L-selenomethionine (SeM), a potential cancer chemopreventive agent, on the gene expression profile of the cultured cell clones. Following a three-day incubation period with SeM, total RNA was extracted, and the gene expression profile was evaluated using Affymetrix human HG U133A microarrays and analyzed by ViaLogy's (Altadena, CA) VMAxS platform deploying quantum resonance interferometry (QRI) processing. The differentially expressed genes and corresponding biological processes were compared across the different treatments and cell types. Whereas SeM significantly affected RNA-DNA metabolism and protein transport and metabolism in all of the cell types evaluated, significant effects of SeM on genes mainly involved in the pathways of cell cycle, growth, differentiation, and apoptosis were observed only in the cell clone with a more malignant phenotype.




Selenium effects on prostate cell growth.
Menter DG, Sabichi AL, Lippman SM.Department of Clinical Cancer Prevention, The University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.

Epidemiological and clinical data suggest that selenium may prevent prostate cancer, but the biological effects of selenium on normal or malignant prostate cells are not well known. We evaluated the effects of sodium selenite (Na2SeO3) or l-selenomethionine (SeMet) on monolayer and anchorage-independent growth in a series of normal primary prostate cultures (epithelial, stromal, and smooth muscle) and prostate cancer cell lines (LNCaP, PC-3, and DU145). We observed differential, dose-dependent growth inhibition and apoptosis within prostate cancer cells (compared with normal prostate cells) treated with 1-500 microM of Na2SeO3 or SeMet. Na2SeO3 more potently inhibited growth at any given concentration. The androgen-responsive LNCaP cells were the most sensitive to selenium growth suppression (IC50s at 72 h for Na2SeO3 and SeMet were 0.2 and 1.0 microM, respectively). Growth of the primary prostate cells virtually was not suppressed (IC50s at 72 h for Na2SeO3 and SeMet were 22-38 and >500 microM, respectively). We also observed that DNA condensation and DNA fragmentation (terminal deoxynucleotidyltransferase dUTP nick end labeling/fluorescence-activated cell sorting) were elevated in selenium-treated cells and that activated caspase-3 colocalized with terminal deoxynucleotidyltransferase dUTP nick end labeling-stained cells by immunofluorescence. Higher basal poly(ADP-ribose) polymerase (PARP) expression levels and PARP cleavage (a substrate for caspase-3) were observed during apoptosis in tumor cells, compared with normal cells. Selective tumor cell death was associated with an increase in sub-G0-G1 cells after propidium iodide staining and fluorescence-activated cell sorting analysis. SeMet caused an increase in arrest in the G2-M phase of the cell cycle selectively in cancer cells. Inhibition of cancer cell growth by SeMet was associated with phosphorylation of P-Tyr15-p34/cdc2, which caused growth arrest in the G2-M phase. Anchorage-independent growth of prostate cancer cells in soft agar was sensitive to selenium. Our results suggest that Na2SeO3 is the more potent inducer of apoptosis in normal and cancer prostate cells. Our SeMet results involving PARP and G2-M cell-cycle arrest (cited above) indicate that SeMet selectively induces apoptosis in cancer but not primary cells of the human prostate. Our overall findings are relevant to the molecular mechanisms of selenium actions on prostate carcinogenesis and help demonstrate the selective, dose-dependent effects of selenium (especially SeMet) on prostate cancer cell death and growth inhibition.

#2 pycnogenol

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Posted 02 March 2009 - 04:12 PM

I thought the best form was Se-methylselenocysteine but I'm really not 100% sure about that.

I occasionally take the Life Extension brand Super Selenium Complex which contains:

Selenium 200 mcg (as SelenoPure L-selenomethionine, sodium selenate, selenodiglutathione, Se-methylselenocysteine)
Vitamin E 30 IU (as D-alpha tocopheryl succinate)

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#3 balance

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Posted 02 March 2009 - 09:58 PM

http://aor.ca/html/products.php?id=104

Go to Articles and then read the 2003 Selenium document. It shows that Se-methylselenocysteine is the best and only form you need and want. Least toxic. Best anti-cancer. And you only need 55mcg for it.

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#4 pycnogenol

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Posted 03 March 2009 - 04:38 PM

http://aor.ca/html/products.php?id=104

Go to Articles and then read the 2003 Selenium document. It shows that Se-methylselenocysteine is the best and only form you need and want. Least toxic. Best anti-cancer. And you only need 55mcg for it.


Here is the PDF link to it:

http://aor.ca/assets...2003_Spring.pdf




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