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SeMet

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SeMet

$28.45 CAD

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AOR CODE: AOR04018

A superior form of selenium

  • Supports normal cell growth and development

  • Promotes the production of glutathione, the body’s most powerful antioxidant

  • Supports proper immune function 

Use this product for: Hormonal Health
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Details

SeMet contains selenomethionine, a natural form of the mineral selenium that is the prominent form which the body absorbs from food sources. It is the main form of selenium that is stored in the body, is more effectively used than other forms and is absorbed 1.5-2 times better than selenite, a form commonly found in supplements. 

Selenium levels of plant-based foods are unpredictable as they will vary with soil selenium content, making it important to supplement with the absorbable and efficient form of selenium to obtain its health benefits. Selenium is necessary for immune function, supporting the production of glutathione, a powerful antioxidant, and boosting immune cell activity. Supplementing with selenium is important for those who want to promote a healthy immune system and normal cell growth especially as selenium soil content is depleted in many areas of North America.

Label Info

Discussion

SeMet is selenium, a trace mineral found in plants such as broccoli and garlic when grown in exceedingly rich soil. Selenium is an antioxidant for the maintenance of good health.

Product Variation

Product Code NPN Size
AOR04018 80015756 90 VEGI-CAPS

Supplements Facts

Serving Size: 1 Capsule Amount % Daily
Selenium (Selenomethionine) 55 mcg

microcrystalline cellulose, dicalcium phosphate, sodium stearyl fumarate. Capsule: hypromellose.

Guarantees

AOR™ guarantees that all ingredients have been declared on the label. Contains no wheat, gluten, corn, nuts, peanuts, sesame seeds, sulphites, mustard, soy, dairy, eggs, fish, shellfish or any animal byproduct.

Adult Dosage

Take 1 capsule daily with a meal, or as directed by a qualified health care practitioner.

Cautions

None known.  

Source

Pharmaceutical synthesis

Main Application

Cellular growth & differentiation

Antioxidant

Immunity

Disclaimer

The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide or replace medical advice to individuals from a qualified health care professional. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes.

Research

Background

Protection From the Body’s Enemies

SeMet is selenomethionine, a superior form of selenium. Selenium is an important nutrient that is needed for the production of glutathione peroxidase, a powerful antioxidant that helps rid the body of dangerous free radicals. Selenium is also needed for the immune system to function properly. Selenium deficiency lowers important immune factors, and selenium supplementation increases immune defenses.

Your Ally Against Cancer

Selenium is well established as a cancer-fighting nutrient. SeMet works in different ways from other selenium forms. It causes cancer cells to commit cellular suicide without affecting normal cells, as opposed to inorganic selenium which damages both healthy and cancerous cells, leading to toxic cell death. SeMet regulates cellular growth to block cancer cells early on and it can stunt the growth of tumors by cutting off their blood supply.

The Best of the Best

Not all forms of selenium are equal. SeMet is less toxic and more potent than other forms of selenium. Selenium’s cancer-fighting strength is linked to its formation of methylselenol. SeMet is directly and easily converted into this important metabolite, making it the most superior form of selenium available.

 Actions of SeMet: Apoptosis vs Necrosis:

Inorganic selenium kills cancer cells through nonselective damage to the DNA and cell membranes of both healthy cells and cancer cells, leading to toxic cell death (necrosis). SeMet selectively activates cancer cells’ “suicide program” (apoptosis) without damage to healthy cells.

Gene expression: SeMet regulates cellular growth programs, inhibiting cancer cells earlier in the cell cycle than does inorganic selenium.

Angiogenesis: SeMet may also act by cutting off the growing tumor’s blood supply more effectively than the common selenium supplements, without interfering with the growth of blood vessels in normal, healthy tissue.

By any measure, SeMet has proved itself to be a safe and highly effective source of selenium.

 

Research

Anti-Cancer Trace Mineral

Selenium is now well established as a potent cancer-fighting trace mineral. Areas of the world with more selenium-rich soil have lower cancer rates, and a randomized, double-blind, placebo-controlled trial in the 1990s showed that men taking a daily 200 microgram selenium supplement experienced a 37% lower risk of developing new cancer, and a whopping 50% lower risk of cancer death.

Protective Effect Against Cancer

This form of selenium has been shown to be effective in fighting cancer. In one human trial involving 238 patients with mild or moderate esophageal squamous dysplasia were supplemented with 200mcg of selenomethionine and/or 200mg of the drug celecoxib twice daily for 10 months. After 10 months it was found that although neither selenomethionine nor celecoxib inhibited esophageal squamous carcinogenesis for all high-risk subjects, supplementation with selenomethionine did have a protective effect among subjects with mild esophageal squamous dysplasia at baseline.

Selenium and colorectal cancer reduction in smokers

A study which was coordinated by the National Cancer Institute (NCI) and carried out in a number of medical centres investigated the relationship between advanced colorectal adenoma in smokers and their serum selenium levels. The results indicated that having higher serum selenium levels could reduce the risk of advanced colorectal smokers especially in recent smokers. This study was published in the Cancer Epidemiology, Biomarkers and Prevention (15, 2:315-20, 2006).

A total of 758 participants were selected and had a least one advanced adenoma of the distal colon; the control subjects had a negative sigmoidscopy. There was a notable inverse association between serum selenium and colorectal adenoma (advanced stage) within the group of recent smokers. No relationship existed between adenoma risk and serum selenium in nonsmokers and previous smokers who had quit smoking over 10 years prior. The study results indicated that selenium may reduce the risk of advanced colorectal adenoma development, especially in the recent smoker high-risk group.

Methylselenol Formation is the Key

But not all forms of selenium are equal in their cancer-fighting properties. To everyone’s surprise, the last decade of scientific research has found that selenium’s anticancer effect is not due to its use as part of antioxidant or detoxifying compounds in the body. It’s also not linked to absolute tissue levels of selenium achieved by a given form of selenium, or to its ability to boost the immune system. Instead, the cancer-fighting potency of any form of selenium is linked to its ability to form methylselenol, a critical selenium metabolite in the body.

Selenomethionine: Organic Over Inorganic

Organic forms of selenium, like selenomethionine are directly and easily converted into this key cancer-fighting metabolite by enzymes in the body called methioninases. In contrast, conventional inorganic (selenite or selenate) selenium supplements are not easily converted to methylselenol. Selenomethionine has also been shown to be a very safe form of selenium. It provides a natural, stable and easily absorbed form of the mineral. As a result, SeMet is simultaneously more potent in its cancer-battling prowess, and less toxic per unit of cancer-fighting punch, than other forms of selenium.

SeMet is a natural form of selenium, and is estimated to make up about half of the selenium obtained from dietary sources. It is the main form in which the body stores selenium, and is easily used by the body and has been shown to have a bioavailability at least 1.5 – 2 times higher than inorganic forms of selenium.

 

Market Trends

Selenium supplements offer antioxidant protection and may help to promote healthy cell differentiation. Not all forms of selenium are equal, as some carry a higher risk of toxicity than others, while others produce more effective metabolites for various purposes. Some of the least toxic forms of selenium with the most cancer-fighting potential include methylselenocysteine and selenomethionine.

AOR Advantage

AOR offers selenium in the form of selenomethionine, a less toxic and more potent form of selenium. Selenium’s cancer-fighting strength is linked to its formation of methylselenol. SeMet is directly and easily converted into this important metabolite, making it one of the most superior form of selenium available. AOR’s SeMet comes in the RDA of 55 mcg per capsule with 90 capsules per bottle, allowing for flexible dosing options.

References

Ip C, Hayes C, Budnick RM, Ganther HE. “Chemical form of selenium, critical metabolites, and cancer prevention.” Cancer Res 1991 Jan 15; 51(2): 595-600.

Ip C. “Lessons from basic research in selenium and cancer prevention.” J Nutr. 1998 Nov; 128(11): 1845-54.

Limburg P.J. et al. “Randomized, Placebo-Controlled, Esophageal Squamous Cell Cancer Chemoprevention Trial of Selenomethionine and Celecoxib.” Gastroenterology. 2005. 129(3): 863-873.

Schrauzer G.N. “Selenomethionine: A Review of Its Nutritional Significance, Metabolism and Toxicity. Journal of Nutrition”. 2000. 130: 1653-1656.

Spallholz J.E. et al.  Methioninase and selenomethionine but not Se-methylselenocysteine generate methylselenol and superoxide in an in vitro chemiluminescent assay: implications for the nutritional carcinostatic activity of selenoamino acids. Biochemical Pharmacology. 2004. 67(3): 547-554.

Whanger PD. “Selenocompounds in plants and animals and their biological significance.” J Am Coll Nutr. 2002 Jun; 21(3): 223-32.

 

Abstract

Randomized, Placebo-Controlled, Esophageal Squamous Cell Cancer Chemoprevention Trial of Selenomethionine and Celecoxib

Gastroenterology. 2005. 129(3): 863-873.

Limburg P.J. et al.

Background & Aims: Esophageal squamous cell carcinoma remains a leading cause of cancer death worldwide. Squamous dysplasia, the accepted histological precursor for esophageal squamous cell carcinoma, represents a potentially modifiable intermediate end point for chemoprevention trials in high-risk populations.

Methods: We conducted a randomized, controlled trial of selenomethionine 200 μg daily and/or celecoxib 200 mg twice daily (2 × 2 factorial design) among residents of Linxian, People’s Republic of China. Subjects had histologically confirmed mild or moderate esophageal squamous dysplasia at baseline. Esophagogastroduodenoscopy was performed before and after a 10-month intervention. Per-subject change (regression, stable, or progression) in the worst dysplasia grade was defined as the primary end point. Results were compared by agent group (selenomethionine vs placebo; celecoxib vs placebo).

Results: Two hundred sixty-seven subjects fulfilled all eligibility criteria, and 238 (89%) completed the trial. Overall, selenomethionine resulted in a trend toward increased dysplasia regression (43% vs 32%) and decreased dysplasia progression (14% vs 19%) compared with no selenomethionine (P = .08). In unplanned stratified analyses, selenomethionine favorably affected a change in dysplasia grade among 115 subjects with mild esophageal squamous dysplasia at baseline (P = .02), but not among 123 subjects with moderate esophageal squamous dysplasia at baseline (P= 1.00). Celecoxib status did not influence changes in dysplasia grade overall (P = .78) or by baseline histology subgroup.

Conclusions: After a 10-month intervention, neither selenomethionine nor celecoxib inhibited esophageal squamous carcinogenesis for all high-risk subjects. However, among subjects with mild esophageal squamous dysplasia at baseline, selenomethionine did have a protective effect. Although it is based on unplanned stratified analyses, this finding is the first report of a possible beneficial effect for any candidate esophageal squamous cell carcinoma chemopreventive agent in a randomized controlled trial

 

Methioninase and selenomethionine but not Se-methylselenocysteine generate methylselenol and superoxide in an in vitro chemiluminescent assay: implications for the nutritional carcinostatic activity of selenoamino acids.

Biochemical Pharmacology. 2004. 67(3): 547-554.

Spallholz J.E. et al.

Methylselenol from selenium metabolism is postulated to be and most experimental evidence now indicates that it is the selenium metabolite responsible for the dietary chemoprevention of cancers. Using the recombinant enzyme methioninase, methylselenol-generating chemiluminesence by superoxide (O2√−) is shown to be catalytically produced from -selenomethionine and , -selenoethionine, but not from methionine or -Se-methylselenocysteine (SeMC). Methylselenol enzymaticaly generated by methioninase activity from the substrate selenomethionine arises from an initial putative selenium radical as measured by chemiluminesence in the absence of glutathione (GSH). In the presence of GSH, superoxide was generated as measured by chemiluminesence and superoxide dismutase inhibition of chemiluminescence. Ascorbic acid also quenched the chemiluminesence from the activity of methioninase with selenomethionine. Methylselenol and other redox cycling selenium compounds are almost assuredly accountable for inducing cell-cycle arrest and apoptosis in cancer cells in vitro and in vivo. Methylselenol generated from selenomethionine by methioninase is catalytic alone in oxidizing thiols, i.e. GSH, generating superoxide and inducing oxidative stress in direct proportion to its concentration. Se-methylselenocysteine in vivo is very likely carcinostatic in like manner to selenomethionine by generating methylselenol from other enzymatic activity, i.e. beta-lyase or amino acid oxidases.

 

Selenocompounds in plants and animals and their biological significance.

J Am Coll Nutr 2002 Jun; 21(3): 223-32.

Whanger PD. 

There are several selenocompounds in tissues of plants and animals. Selenate is the major inorganic selenocompound found in both animal and plant tissues. Selenocysteine is the predominant selenoamino acid in tissues when inorganic selenium is given to animals. Selenomethionine is the major selenocompound found initially in animals given this selenoamino acid, but is converted with time afterwards to selenocysteine. Selenomethionine is the major selenocompound in cereal grains, grassland legumes and soybeans. Selenomethionine can also be the major selenocompound in selenium enriched yeast, but the amount can vary markedly depending upon the growth conditions. Se-methylselenocysteine is the major selenocompound in selenium enriched plants such as garlic, onions, broccoli florets and sprouts, and wild leeks.

 

Caspases as key executors of methyl selenium-induced apoptosis (anoikis) of DU-145 prostate cancer cells.

Cancer Res 2001 Apr 1; 61(7): 3062-70.

Jiang C, Wang Z, Ganther H, Lu J.

Apoptosis induction may be a mechanism mediating the anticancer activity of selenium. Our earlier work indicated that distinct cell death pathways are likely involved in apoptosis induced by the CH3SeH and the hydrogen selenide pools of selenium metabolites. To explore the role of caspases in cancer cell apoptosis induced by selenium, we examined the involvement of these molecules in the death of the DU-145 human prostate carcinoma cells induced by methylseleninic acid (MSeA), a novel penultimate precursor of the putative critical anticancer metabolite CH3SeH. Sodium selenite, a representative of the genotoxic selenium pool, was used as a reference for comparison. The results show that MSeA-induced apoptosis was accompanied by the activation of multiplecaspases (caspase-3, -7, -8, and -9), mitochondrial release of cytochrome c (CC), poly(ADP-ribose) polymerase (PARP) cleavage, and DNA fragmentation. In contrast, selenite-induced apoptotic DNA fragmentation was observed in the absence of these changes, but was associated with the phosphorylation of c-Jun-NH2-terminal kinase 1/2 and p38 mitogen-activated protein kinase/stress-activated protein kinase 2. A general caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-(OMe) fluoromethyl ketone, blocked MSeA-induced cleavage of procaspases and PARP, CC release, and DNA nucleosomal fragmentation, but did not prevent cell detachment. Furthermore, PARP cleavage and caspase activation were confined exclusively to detached cells, indicating that MseA induction of cell detachment was a prerequisite for caspase activation and apoptosis execution. This process therefore resembled “anoikis,” a special mode of apoptosis induction in which adherent cells lose contact with the extracellular matrix. Additional experiments with irreversible caspase inhibitors show that MSeA-induced anoikis involved caspase-3- and -7-mediated PARP cleavage that was initiated by caspase-8 and probably amplified through CC-caspase-9 activation and a feedback activation loop from caspase-3. Taken together, the data support a methyl selenium-specific induction of DU-145 cell apoptosis that involves cell detachment as a prerequisite (anoikis) and is executed principally through caspase-8 activation and its cross-talk with multiple caspases.

 

Selenomethionine: A Review of Its Nutritional Significance, Metabolism and Toxicity.

Journal of Nutrition. 2000. 130: 1653-1656.

Schrauzer G.N.

Although the need for selenium in human and animal nutritionis well recognized, the question concerning the proper formof selenium for supplemental use is still being debated. Ideally,selenium should be supplemented in the form in which it occursnaturally in foods. Because the L-isomer of selenomethionine(Se-met) is a major natural food-form of selenium, syntheticL-Se-met or enriched food sources thereof such as selenium yeastare appropriate supplemental forms of Se for humans; for animals,DL-Se-met is acceptable. Ingested Se-met is either metabolizeddirectly to reactive forms of selenium or stored in place ofmethionine in body proteins. Se-met metabolism is closely linkedto protein turnover. At constant intakes in the nutritionalrange, tissue Se levels increase until a steady state is established,preventing the build-up to toxic levels.

 

Lessons from basic research in selenium and cancer prevention.

J Nutr 1998 Nov; 128(11): 1845-54.

Ip C.

The article reviews the progress in basic research of selenium and cancer prevention during the past decade. Special emphasis is placed on the following four major areas of discussion: 1) chemical forms of selenium and anticarcinogenic activity; 2) selenium-enriched food; 3) in vitro effects of selenite vs. monomethylated selenium; and 4) aromatic selenium compounds. It is clear that basic research has contributed new knowledge to our understanding of selenium biochemistry, anticancer efficacy and regulation of cell growth. Some of this information could be ready for incorporation into the design of a second-generation selenium trial in humans.

 

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