Selenium is a trace mineral with potent antioxidant effects, essential in detoxification processes. It is an important component in sulfur-bearing amino acid production and fetal development during pregnancy. it has gained recent clinical evidence of cancer preventative properties.
Selenium is an essential mineral found in minute amounts in the body. It is one of the essential body substances that can be used in a preventive manner for many diseases including cancer, atherosclerosis, stroke, cirrhosis, arthritis and emphysema. Selenium functions either alone or with enzymes. It is a natural antioxidant that protects against free radicals, spares vitamin E and appears to preserve elasticity of tissue that becomes less elastic with aging. All diseases that are associated with aging are affected by the workings of Selenium.
Selenium may be beneficial in abnormal PAP-smears, cancer prevention, compromised immune system such as in HIV/AIDS, hypothyroidism, osteoarthritis, mood disorders and depression, infertility, allergic rhinitis, macular degeneration, heart disease, atherosclerosis and rheumatoid arthritis.
Published Clinical Studies
The nutritional significance, metabolism and toxicology of selenomethionine.
Schrauzer GN.
Biological Trace Element Research Institute, 2400 Boswell Rd., Suite 200, Chula Vista, CA 91914, USA.
SeMet is a naturally occurring toxic amino acid but at the same time represents the major nutritional source of selenium for higher animals and humans. The ability of SeMet to be incorporated into the body proteins in place of Met furthermore provides a means of reversible Se storage in organs and tissues. This property is not shared by any other naturally occurring selenoamino acid and thus could be associated with a specific physiological function of SeMet. Since higher animals cannot synthesize SeMet, yet from it all needed forms of Se are produced, SeMet meets the criteria of an essential amino acid. Accordingly, SeMet, or enriched food sources thereof, are appropriate forms of Se for human nutritional Se supplementation. However, while SeMet or Se yeast are already widely used in over-the-counter nutritional supplements, infant formulas and parenteral feeding mixtures still contain Se in the form of sodium selenate or sodium selenite, even though these are not the normal nutritional forms of Se. In animal nutrition, these inorganic selenium salts are increasingly replaced by food sources of SeMet such as Se yeast. Synthetic SeMet could also be employed as a feed additive, but its regulatory status is as yet undetermined. The optimal nutritional levels of SeMet for different animal species still need to be determined. The expectation is that lower additions to feedstock of equivalent levels of SeMet will suffice to achieve adequacy than currently approved maximum levels of Se in the form of inorganic Se salts.
Publication Types:
PMID: 14639782 [PubMed - indexed for MEDLINE
Coxsackievirus B3-resistant mice become susceptible in Se/vitamin E deficiency.
Beck MA, Williams-Toone D, Levander OA.
Departments of Nutrition and Pediatrics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7220, USA. melinda_beck@unc.edu
The severity of the heart damage caused by a coxsackievirus infection in mice is determined by several factors, including the genotype of the infecting virus as well as the genetic background of the infected host. Earlier work by us showed that the cardiovirulence of a given coxsackievirus genotype could be increased substantially by feeding the host a diet nutritionally deficient in either selenium or vitamin E. Here we report that host genetic background as a determinant of viral infection outcome is superseded by feeding the host a diet nutritionally deficient in both selenium and vitamin E. Mice of the C57Bl/6 strain, normally resistant to coxsackievirus B3-induced myocarditis, become susceptible when fed such a doubly deficient diet. Our results demonstrate the powerful influence of host nutritional status on the course of viral infection compared to other variables traditionally considered to play major roles in determining the extent of virally induced inflammatory heart disease.
PMID: 12726914 [PubMed - indexed for MEDLINE]
Effect of dietary selenite on N-nitrosodiethylamine-induced and phenobarbital promoted multistage hepatocarcinogenesis in rat: reflection in some minerals.
Thirunavukkarasu C, Sakthisekaran D.
Department of Medical Biochemistry, Dr. ALM Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, 600 113, Chennai, India.
Selenium (Se), a dietary micronutrient, plays a vital role in cancer chemotherapy in many organs including the liver. We have studied the relationship between some minerals, which are essential in normal functioning of cells and anticancer effect of Se in N-nitrosodiethylamine (DEN) induced and phenobarbital (PB) promoted multistage hepatocarcinogenesis. Se (4 ppm through drinking water; as sodium selenite) was given to animals throughout the study, before initiation and during promotion phase of hepatocarcinogenesis, in a defined experimental protocol. Se, sodium, potassium, calcium and iron were measured either in hepatoma, or surrounding liver tissue or whole liver tissue and serum of experimental animals. DEN and PB treatment significantly (P < 0.001) increased potassium, calcium and iron levels in serum, while it decreased (P < 0.001) the Se and sodium levels when compared with control rats. We have also observed significantly increased (P < 0.001) sodium, calcium and iron levels in hepatoma and surrounding liver tissue, whereas, Se, and potassium level was found to be decreased (P < 0.001) when compared with control rats. Supplementation of selenite throughout the study, before initiation and during promotion stage significantly alters the above mineral content. Results showed that the most significant beneficial effect of selenium during hepatocarcinogenesis was exerted potentially in long-term continuous and/or before the initiation phase of carcinogenicity, rather than in the promotion phase. The present and previous results from our laboratory suggest that sub-optimal intake of a single trace mineral can have broad effects on chemotherapy, providing a framework for understanding the multiple beneficial effects of selenium in cancer chemoprevention.
PMID: 14652167 [PubMed - indexed for MEDLINE]
Review of vitamin E and selenium in the prevention of prostate cancer: implications of the selenium and vitamin E chemoprevention trial.
Pak RW, Lanteri VJ, Scheuch JR, Sawczuk IS.
Hackensack University Medical Center, 20 Prospect Avenue, Suite 703, Hackensack, NJ 07601, USA.
The National Cancer Institute in cooperation with the Southwest Oncology Group has begun one of the largest prostate cancer prevention studies to date, the Selenium and Vitamin E Chemoprevention Trial (SELECT). The purpose of this article is to review the evidence and discuss the individual antioxidant compounds under study. The authors comprehensively reviewed the peer-reviewed literature on the chemoprevention of prostate cancer with emphasis on the antioxidants vitamin E and selenium. The credible leads for the primary prevention of prostate cancer using selenium and vitamin E have emerged as secondary findings from randomized controlled trials with corroborative evidence from observational and in vitro studies. Selenium and vitamin E are widely available compounds that are safe if taken in moderation, with relatively few adverse effects. The evidence in support of the antioxidants in the primary prevention of prostate cancer is promising, and the next step in definitively answering the question has been addressed by the investigators of SELECT. The SELECT study will define the role of the antioxidants selenium and vitamin E in the prevention of prostate cancer; complete data from the study will be available in 12 years.
PMID: 14664728 [PubMed - in process]
[Effects of sodium selenite on telomerase activity and telomere length]
Liu Q, Wang H, Hu DC, Ding CJ, Xiao H, Xu HB, Shu BH, Xu SQ.
Department of Chemistry, Huazhong University of Science and Technology, Wuhan 430074, China.
To study the biological basis of selenium in resisting senescence through its effects on cellular telomerase activity and telomere length. In the experiments, the cell line of hepatocytes L-02 was divided into three groups supplemented with sodium selenite at final concentrations of 0, 0.5 and 2.5 micromol/L, respectively. Cellular telomerase activity was measured by telomeric repeat amplification protocol and enzymatic luminometric inorganic pyrophosphate detection assay. RT-PCR was used to semi-quantitatively detect human telomerase reverse transcriptase (hTERT) gene expression. The change of telomere length was assayed through flow cytometry and fluorescence in situ hybridization. Results showed that L-02 cells had low telomerase activity and hTERT gene expression level when cultured in the normal way. The cells grew well after 3-week-cultivation in the media supplemented with 0.5 or 2.5 micromol/L sodium selenite. Besides, sodium selenite significantly increased cellular telomerase activity and hTERT gene expression level. The telomere length of L-02 cells was also extended after 4-week-cultivation with sodium selenite. Thus, sodium selenite at nutritional doses could prolong the life span of hepatocytes L-02 through increasing telomerase activity and telomere length. This result provides a possible mechanism for explaining the anti-senescence function of selenium.
PMID: 14673504 [PubMed - in process]
Selenium supplementation and lung cancer incidence: an update of the nutritional prevention of cancer trial.
Reid ME, Duffield-Lillico AJ, Garland L, Turnbull BW, Clark LC, Marshall JR.
Roswell Park Cancer Institute, Buffalo, NY 14263, USA.
Interest in the chemopreventive effects of the trace element selenium has spanned the past three decades. Of >100 studies that have investigated the effects of selenium in carcinogen-exposed animals, two-thirds have observed a reduction in tumor incidence and/or preneoplastic endpoints (G. F. Combs and S. B. Combs, The Role of Selenium in Nutrition Chapter 10, pp. 413-462. San Diego, CA: Academic Press, 1986, and B. H. Patterson and O. A. Levander, Cancer Epidemiol. Biomark. Prev., 6: 63-69, 1997). The Nutritional Prevention of Cancer Trial, a randomized clinical trial reported by Clark et al. (L. C. Clark et al., JAMA, 276: 1957-1963, 1996), showed as a secondary end point, a statistically significant decrease in lung cancer incidence with selenium supplementation. The adjusted hazard ratio (HR) was 0.56 [95% confidence interval (CI), 0.31-1.01; P = 0.05]. These results were based on active follow-up of 1312 participants. This reanalysis used an extended Nutritional Prevention of Cancer Trial participant follow-up through the end of the blinded clinical trial on February 1, 1996. The additional 3 years added 8 cases to the selenium-treated group and 4 cases to the placebo group, and increased follow-up to 7.9 years. The relative risk of 0.70 (95% CI, 0.40-1.21; P = 0.18) is not statistically significant. Whereas the overall adjusted HR is not significant (HR = 0.74; 95% CI, 0.44-1.24; P = 0.26), and the HR for current and former smokers was not significant, the trend is toward a reduction in risk of incident lung cancer with selenium supplementation. In a subgroup analysis there was a nominally significant HR among subjects with baseline plasma selenium in the lowest tertile (HR = 0.42; 95% CI, 0.18-0.96; P = 0.04). The analysis for the middle and highest tertiles of baseline showed HRs of 0.91 and 1.25. The current reanalysis indicates that selenium supplementation did not significantly decrease lung cancer incidence in the full population, but a significant decrease among individuals with low baseline selenium concentrations was observed.
Publication Types:
PMID: 12433704 [PubMed - indexed for MEDLINE]
Clark LC, Dalkin B, Krongrad A, et al. Decreased incidence of prostate cancer with selenium supplementation: results of a double-blind cancer prevention trial. Br J Urol 1998;81:730-4.