An overall intake (foods and supplements) in the range of 200-300ug daily should be the goal for general health and well being with an emphasis on anti-carcinogenic properties.
An Essential Mineral that is heralded for its anti-oxidant capabilities, it forms a part of some anti-oxidant enzymes such as glutathione to confer protective effects. Taking more than needed, however, can cause oxidative damage and may be pro-diabetic.
This page features 96 unique references to scientific papers.
Follow this Page for updates
The Human Effect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what effects selenium has on your body, and how strong these effects are.
|Grade||Level of Evidence|
|Robust research conducted with repeated double-blind clinical trials|
|Multiple studies where at least two are double-blind and placebo controlled|
|Single double-blind study or multiple cohort studies|
|Uncontrolled or observational studies only|
Level of Evidence
? The amount of high quality evidence. The more evidence, the more we can trust the results.
Magnitude of effect
? The direction and size of the supplement's impact on each outcome. Some supplements can have an increasing effect, others have a decreasing effect, and others have no effect.
Consistency of research results
? Scientific research does not always agree. HIGH or VERY HIGH means that most of the scientific research agrees.
|Pre-Eclampsia Risk||Notable||Very High See all 3 studies|
|Prostate Cancer Risk||Minor||- See study|
|Acne||Minor||- See study|
Table of Contents:
- 1 Sources and Composition
- 2 Interactions with Glucose Metabolism
- 3 Interactions with Cancer Metabolism
Interactions with Aesthetics
- 4.1 Skin
- 5 Other Medical Conditions
- 6 Safety and Toxicity
Selenium is an essential trace mineral that can be found in organic and inorganic forms. The primary organic forms are the selenoamino acids, selenocysteine, selenomethione, and Se-methylselenocysteine. The main active dietary form is selenomethionine. Other notable organic forms are selenoneine, which is the major form in tuna , and γ-glutamyl-Se-selenomethyl-selenocysteine, which is found in a variety of plant foods.
Selenite and selenate, the inorganic forms found in soil and water, are used by plants and animals to synthesize the organic forms. Plants mainly synthesize selenomethionine, whereas animal synthesis of selenomethionine from selenite is negligible, with synthesis of selenocysteine being more viable.
The selenium content of food correlates with the total protein content due to the ability of Se-amino acids to replace sulfur in proteins, although there are many notable exceptions depending on the physiology of the organism. Intake varies considerably by region depending on the levels in soil, the growing conditions of crops, the diets of livestock, and the local diet.
Brazil nuts contain the most selenium per gram of any measured food; two Brazil nuts daily for 12 weeks has been observed to increase serum selenium levels by 64.2% in adults from New Zealand. Other nuts and seeds provide more modest amounts of selenium, with Greek sesame seeds being a known region-specific exception, showcasing the extreme variability by region.
Selenium is consistently high in seafood and generally high in meats and eggs, although subject to variation depending on feed and animal supplementation. Dairy, particularly cheese, is also a significant source, with selenium content being inversely correlated with the fat content
Legumes such as lentils can be notable sources but vary depending on the species of legume. Wheat flour used in bread and pasta also provides nutritionally important amounts of selenium. Vegetables and fruits are not usually significant sources of selenium, however there are reports of Indian onions and portobello mushrooms being potent sources.
A wide variety of foods can supply significant amounts of selenium, with fish and Brazil nuts being the most consistent sources.
It normally acts in concert with a class of enzymes and transporters called Selenoproteins (proteins with selenium in them), many of which are intrinsic anti-oxidant enzymes. In these selenoproteins, selenium acts as a prosthetic group or active site. Distinctly, Selenoprotein S is involved in protection against endoplasmic reticulum stress and regulation of proinflammatory cytokine release.
Selenium is essential for the functioning of the iodothyronine deiodinases which catalyze the deiodination of thyroid hormones, converting T4 to T3 and rT3, with implications for growth and thermogenesis.
In thioredoxin reductases it plays a role in redox reactions that control transcription factors, cell proliferation and apoptosis. Thioredoxin reductases can also reduce dehydroascorbic acid, an oxidized form of ascorbic acid.
RDA is based on the amount of selenium required to maximize the activity of glutathione peroxidase (GPx) in serum. Due to inadequate evidence in infants, an adequate intake (AI) is set based on the average intake, primarily from breast milk. This is 15ug/day from 0-6 months of age and 20ug from 7-12 months. The RDAs are 20ug/day from age 1-3, 30ug from 4-8, 40ug from 9-13, and 55ug for 14 and older, with no differences between males and females. The RDAs for pregnant and breastfeeding women are 60ug and 70ug, respectively.
Deficiency of Selenium occurs when overall intake is less than 11ug, and 40ug is typically recommended as the minimum intake. Selenium deficiency in children can result in Keshan disease, named for the county in China where where patients exhibited a severe and often fatal form of cardiomyopathy. Keshan disease is correlated with selenium intake, status, and GPx activity; supplementation of selenium reduces its incidence. There is a likely role of various viral infections, which are likely exacerbated by selenium deficiency.
Intake of 55ug is sufficient to support the needs of 25 selenoproteins although there may be some interindividual differences. Levels above this, but not yet into therapeutic dosages (200-300ug) are possibly in the range of what is needed to exert anti-carcinogenic effects and doses up to the range of 750-800ug daily seem to be relatively free of harm. Dosages of 1,500-1,600ug or above start to become associated with harm and doses nearing 3,000-5,000ug can cause direct DNA damage.
Non-organic forms typically revolve around Selenite, a triple-oxidized form of selenium. It can be converted via Glutathione into Selenade; this multiple step process produces some superoxide radicals.
Organic forms include the selenoamino acids, which include selenocysteine, selenomethione, and Se-methylselenocysteine. The main active dietary form is selenomethionine. Selenomethionine is a relatively stable compound, but has pro-oxidative metabolites such as Selenid and Methylselenol.
Selenium metabolites can also regulate cell cycles and apoptosis, and aid in tumor regulation.
The synthetic form called MethylSelenic Acid can be directly reduced into methylselenol and can avoid the B-lysase enzyme intermediate commonly seen with dietary selenium.
Selenium has been noted in the past to aid glucose metabolism by acting as an insulin mimetic and thus, aiding the deposition of glucose into both fat and muscle cells. These effects have also been seen in vivo.
In populations that have sufficient selenium status, epidemiological research and one intervention have suggested that further supplementation may increase the risk for insulin resistance and type 2 diabetes. The intervention was dosed at 200mcg daily.
The theorized mechanism of action is that after a certain threshold of selenium intake (past the RDA, nearing the TUL), selenium builds up in pancreatic tissue and exerts oxidative stress on beta-cells that secrete insulin.
This may be an issue of selenium being anti-diabetic acutely (via acting as an insulin-mimetic and aiding in glucose deposition) but over time damaging beta-cells and exerting the opposite effect and being pro-diabetic.
However, one intervention found that supplementation of selenium by pregnant women who were not deficient in selenium, did not result in increases of adiponectin, a marker of insulin resistance. 
Supplementation of selenium for insulin resistance or type 2 diabetes is not recommended due to its possible pro-diabetic effects.
Several studies have found that selenium levels decrease in women during pregnancy due to several phenomena such as increased lipid peroxidation, increased fetal requirement, hemodilutional phenomena, and deposition in the placenta.
A systematic review and meta-analysis, found that selenium concentrations are lower in women with gestational hyperglycemia, when compared to normoglycemic pregnant women.  The same study found that women with gestational diabetes mellitus had lower concentrations of selenium than normal pregnant women in the second and third trimester. However, the differences were only significant in the third trimester. It is believed that this is due to the higher tendency of insulin resistance and higher activity of peroxidase enzymes, such as erythrocyte glutathione peroxidase, in the third trimester.
Women with GDM or impaired glucose tolerance are more likely to be impacted by oxidative stress and more likely to have lower concentrations of selenium. Increasing selenium intake through food or dietary supplements may be beneficial for such populations.
Selenium was first discovered to be related to cancer via correlational research showing higher cancer rates in areas with lower crop selenium content.
Selenoproteins themselves, rather than individual selenoamino acids, are also implicated in cancer prevention. These selenoproteins are typically those that exert anti-oxidative effects (Glutathione Peroxidases and Selenoprotein P) and alleviate cancer during the promotion stage.
Specific selenoproteins that have been investigated for being linked to specific cancers include Glutathione Peroxidase 1 being associated with head and neck, lung and breast, and bladder and prostate cancers, Glutathione Peroxidase 2 being associated with colorectal adenoma, Selenoprotein P being associated with both colorectal adenoma and prostate cancer, Selenoprotein 15 being associated Head, Neck, breast and lung cancer, and Thioredoxin reductase 1 being associated generally with most cancers. Selenium also enhances the effects of tumor protein p53 which promotes DNA repair, apoptosis and inhibits proliferation.
Circulating selenium (independent of supplementation) is associated with a decrease in prostate cancer as assessed by a relatively small meta-analysis in a relatively dose-dependent manner up to a serum concentration of 170ng/mL, where it results in a relative risk ratio of 0.8 relative to 60ng/mL (set as baseline). The same meta-analysis found a decreased risk of prostate cancer associated with toenail selenium levels at up to 1 μg/g, where the risk then rose again.
The Selenium and Vitamin E Cancer Prevention Trial (SELECT) found no association between selenium status (as measured in toenails) and prostate cancer in any of five selenum concentration quintiles in the population, whose selenium levels ranged from 0.48-8.97μg/g (mean 0.89μg/g, 95% CI 0.55-1.43μg/g). Since there were only 13 cancer cases with toenail selenium levels less than 0.617μg/g included in this analysis, this study represents a relatively selenium-replete United States population compared to patients who were in included in the previous meta-analysis.
Higher selenium levels are correlated with a reduced risk of breast cancer.
One meta-analysis, which examined 16 epidemiological studies, found that high selenium concentrations in serum were associated with a significant decrease in the risk of breast cancer (P=0.002), however, no such association was found between risk of breast cancer and selenium concentration in toe nails (P=0.17)
Acne vulgaris is a chronic skin disease characterized by follicular hyperkeratinization, hormonally-mediated sebum overproduction, and chronic inflammation of the pilosebaceous unit. It is believed that the damaging of lipids in the skin via free radicals is responsible for the inflammatory component of acne. Recent research has found that those who suffer from acne are unable to mitigate this damage efficiently because their antioxidant defense system is overwhelmed. 
Thus, based on this research, new studies have aimed to look at the effect of antioxidant supplementation on lesion counts.
A single-blind, placebo-controlled study that aimed to compare silymarin, n-acetylcysteine, and selenium to placebo in reducing lesion counts, found that after eight weeks of supplementation, there was a notable reduction in lesion count in all of the experimental groups, however, the reduction in lesion count was only statistically significant in the n-acetylcysteine and silymarin groups.
Selenium supplementation is not very effective in reducing lesion counts in those who suffer from acne.
Kashin-Beck disease (KBD) is a endemic, degenerative osteoarthropathy, which is mainly distributed from northeastern to southwestern China. It is a disease characterized by enlarged and shortened fingers, arthritic pain, morning stiffness, deformed joints with limited motion in the extremities, excessive apoptosis, and dedifferentiation of chondrocytes.
Several studies have found that KBD is prominent in areas that have soils, plants, animals, and humans that are deficient in selenium. One particular study found that in the Heilongjiang Province in China, the mean serum selenium concentration is roughly 20 ng/L, nearly one-tenth of the mean found in the United States. Such studies have found that KBD is almost exclusive to selenium-poor belts like this. Other studies have found that the severity of KBD in a particular area is closely tied to the selenium content there.
A meta-analysis conducted in 2015, examined twenty-six studies and found that there were significant differences in whole blood selenium levels, serum selenium levels, selenium levels in the hair, and urinary selenium levels between subjects with KBD and healthy controls, with the former having significantly lower levels of selenium on all indicated measures.
Ever since selenium deficiency has been recognized as a possible factor in the onset of KBD, several interventional studies have aimed to look at the effects of selenium supplementation on the incidence of developing KBD, with the majority finding that supplementation reduced the risk of developing KBD.
It is theorized that selenium’s role in preventing the incidence of KBD may be attributed to its ability to protect cartilage tissue from the effects of the T-2 toxin, a mycotoxin found in grains that has been hypothesized to contribute to the onset of KBD.
This possible mechanism likely explains why one epidemiological interventional study found that the experimental groups that were given either selenium-iodine salt or rice from areas where there was no prevalence of KBD, were less likely to develop more X-ray lesions, and more likely to have higher metaphyseal repair rates than the control groups.
KBD is exclusive to areas where foods are contaminated by the T-2 toxin and where there exists a deficiency of selenium. Supplementation of selenium can prevent the onset of KBD and help treat it.
Pre-eclampsia is a disease that affects pregnant women. It is known to be a leading cause of maternal mortality and morbidity worldwide. The disorder is diagnosed by high blood pressure and large amounts of protein in the urine on or after the 20th week of gestation.  In more severe cases of the disorder, there is the presence of systemic endothelial dysfunction, microangiopathy, elevated liver enzymes and red blood cell breakdown. 
An animal study found that pregnant rats that were fed selenium free-diets, prior to and following conception, were found to have significant increases in systolic blood pressure and proteinuria, when compared to pregnant rats fed normal selenium diets (239 μg/kg selenium) or high selenium diets (1000 μg/kg selenium). The rats that were deprived of selenium were also found to have significant decreases in liver glutathione peroxidase and thioredoxin peroxidase. 
Several observational studies have established that women who suffer from pre-eclampsia, have significantly lower levels of selenium plasma and lower toenail selenium concentrations.  Lower levels were also found to be significantly associated with more severe expression of the disorder. 
Serum soluble vascular endothelial growth factor receptor-1 (sFlt-1) is a tyrosine kinase protein and anti-angiogenic factor that is associated with the risk of pre-eclampsia.
A randomized controlled trial, with 230 primiparous pregnant women, found that supplementation of selenium (60 μg/d, as Se-enriched yeast) by the experimental group (n=115), from 12 to 14 weeks of gestation until delivery, resulted in significantly lower concentrations of sFlt-1 when compared to the control group (n=115). 
A double-blind, randomized, placebo-controlled trial found that pregnant women who were given 100 μg of selenium per day, from the first trimester until the day of delivery, were less likely to develop pre-eclampsia, however, this was not found to be significant (p > 0.05). 
A systematic review and meta-analysis, concluded from thirteen observational studies and three randomized control trials, that there exists an inverse association of blood selenium levels and the risk of pre-eclampsia. This review found that supplementation of selenium significantly reduces the incidence of pre-eclampsia (p=0.02).  However, the authors of one of the studies which this meta-analysis uses, have critiqued this interpretation because the authors of the meta-analysis failed to distinguish that there was a significant reduction in selenium concentrations in umbilical venous samples in the pre-eclampsia group. The authors also critiqued several other aspects of the review, stating that the errors would affect the results of the meta-analysis. 
Several observational studies have found that women with lower levels of selenium in their blood are more likely to develop pre-eclampsia than women with adequate levels of Selenium in their blood. Supplementation of selenium has been demonstrated in randomized controlled trials to lower the incidence of pre-eclampsia.
Much danger of excessive selenium comes through the pro-oxidant compound sodium selenite (thrice oxygenated selenium bound to sodium); this compound is able to induce tumor death via its pro-oxidant abilities, but is also toxic to other cells.
In vitro studies noted that high Se intake can be toxic and have adversely effect on the integrity of genomic DNA in various tissues and organs. When human peripheral blood lymphocytes was exposed to high concentrations of two inorganic salts of selenium-sodium selenite (2.9 x 10-5 M) and sodium selenate (2.65 x 10-5 M), it was found to be lethal. One study that examined DNA oxidation in rats suggests that high dietary intake of inorganic selenium may induce DNA damage in the liver. Although the mechanisms responsible for the adverse effects of high doses of Se are not completely understood, the effects can be severe with DNA damage, oxidative stress, and cell death induction.
One clinical trial examined the plasma response and toxicity reports from 24 men with prostate cancer who received either 1600 or 3200 mcg/day of selenized yeast for up to 24 months. The 3200 mcg/day doses produced more symptoms of selenium toxicity (garlic breath, brittle hair and nails, stomach upset, dizziness) than the 1600 mcg/day doses, but these symptoms were not severe and did not correlate with peaks in plasma selenium levels. The study suggests that doses of selenized yeast greater than 400 mcg/day can be given in controlled situations, for extended periods of time, without serious toxicity.
An observational study shows that dietary exposure to selenium compounds of around 300 mcg per day can have early toxic effect on endocrine function, particularly on the synthesis of thyroid hormones, and NK-cell suppression. One clinical trial randomized subjects to 100 mcg, 200 mcg, or 300 mcg selenium-enriched yeast or placebo tablets for 5 years and found that in euthyroid subjects, selenium supplementation decreased serum TSH and FT4 concentrations by 0.066mIU/I and 0.11 pmol/I, respectively, per 100 mcg/day increase.
Human experimental trials have associated selenium intake with an increased risk for type 2 diabetes. One observational study found that after a median follow-up of 16 years, subjects developed diabetes with an average dietary selenium intake of 55.7 mcg/day, with an odds ratio of 1.29 (95% CI: 1.10, 1.52) for diabetes associated with a 10 mcg/day increase in selenium intake. A clinical trial that assigned subjects with type 2 diabetes to 200 μg/day or placebo for 3 months revealed deterioration in blood glucose control and noted a significant increase in fasting plasma glucose by almost 20 mg/dL in the selenium group and a decrease of about 20 mg/dL in the placebo group. Another clinical trial assigned nondiabetic patients to selenium 200 mcg/day or placebo and found that after a follow up of about 7.7 years, selenium supplementation significantly increased the risk for the disease, with a hazard ratio of 1.55 (95% CI, 1.03 to 2.33).
A case report of 201 subjects who ingested a liquid dietary supplement that contained 200 times the labeled concentration of selenium (~41,749 mcg/day) noted symptoms including diarrhea, fatigue, hair loss, joint pain, nail discoloration or brittleness, and nausea. Patients often continued to experience hair and nail changes, memory loss, mood swings, fatigue, muscle pains, and garlic breath 90 days after the exposure to selenium had ended.
Another case of a misformulated dietary supplement which contained over 40,000 mcg of Se examined selenium exposure in 97 subjects through nail sample tests. Subjects self-reported high occurrences of dermatological lesions, muscle and joint pain, and neuropsychological signs and symptoms including fatigue, confusion, memory loss, anxiety, fingertip tingling, depression, anger, irritability, insomnia, dizziness and imbalance, eye and vision problems and headache.
A case of xanthotrichia, or yellow hair discoloration, has been reported with selenium sulfide 2.5% shampoo and dihydroxyacetone.
- Schrauzer GN. Selenomethionine: a review of its nutritional significance, metabolism and toxicity. J Nutr. (2000)
- Yamashita Y, Yabu T, Yamashita M. Discovery of the strong antioxidant selenoneine in tuna and selenium redox metabolism. World J Biol Chem. (2010)
- Winkel LH, et al. Selenium Cycling Across Soil-Plant-Atmosphere Interfaces: A Critical Review. Nutrients. (2015)
- Navarro-Alarcon M, Cabrera-Vique C. Selenium in food and the human body: a review. Sci Total Environ. (2008)
- Thomson CD, et al. Brazil nuts: an effective way to improve selenium status. Am J Clin Nutr. (2008)
- Pappa EC, Pappas AC, Surai PF. Selenium content in selected foods from the Greek market and estimation of the daily intake. Sci Total Environ. (2006)
- Barclay MNI, MacPherson A, Dixon J. Selenium Content of a Range of UK Foods. J Food Compost Anal. (1995)
- Papp LV, et al. From selenium to selenoproteins: synthesis, identity, and their role in human health. Antioxid Redox Signal. (2007)
- Rayman MP. Selenium and human health. Lancet. (2012)
- Mustacich D, Powis G. Thioredoxin reductase. Biochem J. (2000)
- May JM, et al. Reduction of the ascorbyl free radical to ascorbate by thioredoxin reductase. J Biol Chem. (1998)
- Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids.
- Letavayová L, Vlcková V, Brozmanová J. Selenium: from cancer prevention to DNA damage. Toxicology. (2006)
- Chen J. An original discovery: selenium deficiency and Keshan disease (an endemic heart disease). Asia Pac J Clin Nutr. (2012)
- Roman M, Jitaru P, Barbante C. Selenium biochemistry and its role for human health. Metallomics. (2014)
- Stadtman TC. Discoveries of vitamin B12 and selenium enzymes. Annu Rev Biochem. (2002)
- Moghadaszadeh B, Beggs AH. Selenoproteins and their impact on human health through diverse physiological pathways. Physiology (Bethesda). (2006)
- Rayman MP. Selenoproteins and human health: insights from epidemiological data. Biochim Biophys Acta. (2009)
- Rayman MP. Selenium in cancer prevention: a review of the evidence and mechanism of action. Proc Nutr Soc. (2005)
- Combs GF Jr, Clark LC, Turnbull BW. An analysis of cancer prevention by selenium. Biofactors. (2001)
- Schrauzer GN. Nutritional selenium supplements: product types, quality, and safety. J Am Coll Nutr. (2001)
- Reid ME, et al. A report of high-dose selenium supplementation: response and toxicities. J Trace Elem Med Biol. (2004)
- Whanger PD. Selenium and its relationship to cancer: an update. Br J Nutr. (2004)
- Brozmanová J, et al. Selenium: a double-edged sword for defense and offence in cancer. Arch Toxicol. (2010)
- Suzuki KT, Kurasaki K, Suzuki N. Selenocysteine beta-lyase and methylselenol demethylase in the metabolism of Se-methylated selenocompounds into selenide. Biochim Biophys Acta. (2007)
- Seitomer E, et al. Analysis of Saccharomyces cerevisiae null allele strains identifies a larger role for DNA damage versus oxidative stress pathways in growth inhibition by selenium. Mol Nutr Food Res. (2008)
- Ip C, et al. In vitro and in vivo studies of methylseleninic acid: evidence that a monomethylated selenium metabolite is critical for cancer chemoprevention. Cancer Res. (2000)
- Stapleton SR. Selenium: an insulin-mimetic. Cell Mol Life Sci. (2000)
- The Insulin-Like effects of Selenate in Rat Adipocytes.
- Fürnsinn C, et al. Insulin-like vs. non-insulin-like stimulation of glucose metabolism by vanadium, tungsten, and selenium compounds in rat muscle. Life Sci. (1996)
- Ghosh R, Mukherjee B, Chatterjee M. A novel effect of selenium on streptozotocin-induced diabetic mice. Diabetes Res. (1994)
- Laclaustra M, et al. Serum selenium concentrations and diabetes in U.S. adults: National Health and Nutrition Examination Survey (NHANES) 2003-2004. Environ Health Perspect. (2009)
- Stranges S, et al. Effects of long-term selenium supplementation on the incidence of type 2 diabetes: a randomized trial. Ann Intern Med. (2007)
- Selenium and Diabetes: More Bad News for Supplements.
- Fridlyand LE, Philipson LH. Oxidative reactive species in cell injury: Mechanisms in diabetes mellitus and therapeutic approaches. Ann N Y Acad Sci. (2005)
- Introduction: The selenium conundrum.
- Mao J, et al. No effect of modest selenium supplementation on insulin resistance in UK pregnant women, as assessed by plasma adiponectin concentration. Br J Nutr. (2016)
- Kosanovic M, et al. Maternal and fetal cadmium and selenium status in normotensive and hypertensive pregnancy. Biol Trace Elem Res. (2002)
- Molnar J, et al. Serum selenium concentrations correlate significantly with inflammatory biomarker high-sensitive CRP levels in Hungarian gestational diabetic and healthy pregnant women at mid-pregnancy. Biol Trace Elem Res. (2008)
- Kilinc M, et al. Evaluation of serum selenium levels in Turkish women with gestational diabetes mellitus, glucose intolerants, and normal controls. Biol Trace Elem Res. (2008)
- Tan M, et al. Changes of serum selenium in pregnant women with gestational diabetes mellitus. Biol Trace Elem Res. (2001)
- Tara F, et al. Selenium supplementation and the incidence of preeclampsia in pregnant Iranian women: a randomized, double-blind, placebo-controlled pilot trial. Taiwan J Obstet Gynecol. (2010)
- Askari G, et al. The association between serum selenium and gestational diabetes mellitus: a systematic review and meta-analysis. J Trace Elem Med Biol. (2015)
- Shamberger RJ, Frost DV. Possible protective effect of selenium against human cancer. Can Med Assoc J. (1969)
- Spallholz JE, Palace VP, Reid TW. 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. Biochem Pharmacol. (2004)
- Kim A, et al. Methylselenol generated from selenomethionine by methioninase downregulates integrin expression and induces caspase-mediated apoptosis of B16F10 melanoma cells. J Cell Physiol. (2007)
- Valko M, et al. Free radicals and antioxidants in normal physiological functions and human disease. Int J Biochem Cell Biol. (2007)
- Valko M, et al. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem Biol Interact. (2006)
- Valko M, et al. Role of oxygen radicals in DNA damage and cancer incidence. Mol Cell Biochem. (2004)
- Hu YJ, et al. Allelic loss at the GPx-1 locus in cancer of the head and neck. Biol Trace Elem Res. (2004)
- Ichimura Y, et al. Increased risk of bladder cancer associated with a glutathione peroxidase 1 codon 198 variant. J Urol. (2004)
- Hu YJ, Diamond AM. Role of glutathione peroxidase 1 in breast cancer: loss of heterozygosity and allelic differences in the response to selenium. Cancer Res. (2003)
- Moscow JA, et al. Loss of heterozygosity of the human cytosolic glutathione peroxidase I gene in lung cancer. Carcinogenesis. (1994)
- Al-Taie OH, et al. Expression profiling and genetic alterations of the selenoproteins GI-GPx and SePP in colorectal carcinogenesis. Nutr Cancer. (2004)
- Mörk H, et al. Inverse mRNA expression of the selenocysteine-containing proteins GI-GPx and SeP in colorectal adenomas compared with adjacent normal mucosa. Nutr Cancer. (2000)
- Calvo A, et al. Alterations in gene expression profiles during prostate cancer progression: functional correlations to tumorigenicity and down-regulation of selenoprotein-P in mouse and human tumors. Cancer Res. (2002)
- Méplan C, et al. Relative abundance of selenoprotein P isoforms in human plasma depends on genotype, se intake, and cancer status. Antioxid Redox Signal. (2009)
- Hu YJ, et al. Distribution and functional consequences of nucleotide polymorphisms in the 3'-untranslated region of the human Sep15 gene. Cancer Res. (2001)
- Kumaraswamy E, et al. Structure-expression relationships of the 15-kDa selenoprotein gene. Possible role of the protein in cancer etiology. J Biol Chem. (2000)
- Jablonska E, et al. Lung cancer risk associated with selenium status is modified in smoking individuals by Sep15 polymorphism. Eur J Nutr. (2008)
- Lincoln DT, et al. The thioredoxin-thioredoxin reductase system: over-expression in human cancer. Anticancer Res. (2003)
- Gladyshev VN, et al. Contrasting patterns of regulation of the antioxidant selenoproteins, thioredoxin reductase, and glutathione peroxidase, in cancer cells. Biochem Biophys Res Commun. (1998)
- Babaknejad N, et al. The relationship between selenium levels and breast cancer: a systematic review and meta-analysis. Biol Trace Elem Res. (2014)
- Hurst R, et al. Selenium and prostate cancer: systematic review and meta-analysis. Am J Clin Nutr. (2012)
- Kristal AR1, et al. Baseline Selenium Status and Effects of Selenium and Vitamin E Supplementation on Prostate Cancer Risk. J Natl Cancer Inst. (2014)
- Bowe WP, Patel N, Logan AC. Acne vulgaris: the role of oxidative stress and the potential therapeutic value of local and systemic antioxidants. J Drugs Dermatol. (2012)
- Sahib A, et al. Effects of Oral Antioxidants on Lesion Counts Associated with Oxidative Stress and Inflammation in Patients with Papulopustular Acne. J Clin Exp Dermatol Res. (2012)
- Yang L, et al. Selenium and Iodine Levels in Subjects with Kashin-Beck Disease: a Meta-analysis. Biol Trace Elem Res. (2016)
- Yao Y, Pei F, Kang P. Selenium, iodine, and the relation with Kashin-Beck disease. Nutrition. (2011)
- Sun LY, et al. Effects of the consumption of rice from non-KBD areas and selenium supplementation on the prevention and treatment of paediatric Kaschin-Beck disease: an epidemiological intervention trial in the Qinghai Province. Osteoarthritis Cartilage. (2014)
- Eiland E, Nzure C, Faulkner M. Preeclampsia 2012. J Pregnancy. (2012)
- Al-Jameil N, et al. A brief overview of preeclampsia. J Clin Med Res. (2014)
- Vanderlelie J, Venardos K, Perkins AV. Selenium deficiency as a model of experimental pre-eclampsia in rats. Reproduction. (2004)
- Vanderlelie J, Perkins AV. Selenium and preeclampsia: A global perspective. Pregnancy Hypertens. (2011)
- Mistry HD, et al. Reduced selenium concentrations and glutathione peroxidase activity in preeclamptic pregnancies. Hypertension. (2008)
- Farzin L, Sajadi F. Comparison of serum trace element levels in patients with or without pre-eclampsia. J Res Med Sci. (2012)
- Maleki A, et al. The relationship between plasma level of Se and preeclampsia. Hypertens Pregnancy. (2011)
- Rayman MP, Bode P, Redman CW. Low selenium status is associated with the occurrence of the pregnancy disease preeclampsia in women from the United Kingdom. Am J Obstet Gynecol. (2003)
- Rayman MP, et al. Effect of selenium on markers of risk of pre-eclampsia in UK pregnant women: a randomised, controlled pilot trial. Br J Nutr. (2014)
- Xu M, et al. Selenium and Preeclampsia: a Systematic Review and Meta-analysis. Biol Trace Elem Res. (2016)
- Mistry HD, Broughton Pipkin F, Kurlak LO. Letter Regarding: Selenium and Preeclampsia: A Systemic Review and Meta-Analysis. Biol Trace Elem Res. (2016)
- Valdiglesias V, et al. In vitro evaluation of selenium genotoxic, cytotoxic, and protective effects: a review. Arch Toxicol. (2010)
- Biswas S, Talukder G, Sharma A. Chromosome damage induced by selenium salts in human peripheral lymphocytes. Toxicol In Vitro. (2000)
- Wycherly BJ, Moak MA, Christensen MJ. High dietary intake of sodium selenite induces oxidative DNA damage in rat liver. Nutr Cancer. (2004)
- Yang G, Zhou R. Further observations on the human maximum safe dietary selenium intake in a seleniferous area of China. J Trace Elem Electrolytes Health Dis. (1994)
- Steven Morris J, Stampfer MJ, Willett W. Dietary selenium in humans toenails as an indicator. Biol Trace Elem Res. (1983)
- Hunter DJ, et al. Predictors of selenium concentration in human toenails. Am J Epidemiol. (1990)
- van den Brandt PA, et al. Predictors of toenail selenium levels in men and women. Cancer Epidemiol Biomarkers Prev. (1993)
- Longnecker MP, et al. A 1-y trial of the effect of high-selenium bread on selenium concentrations in blood and toenails. Am J Clin Nutr. (1993)
- Vinceti M, et al. Adverse health effects of selenium in humans. Rev Environ Health. (2001)
- Winther KH, et al. Does selenium supplementation affect thyroid function? Results from a randomized, controlled, double-blinded trial in a Danish population. Eur J Endocrinol. (2015)
- Stranges S, et al. A prospective study of dietary selenium intake and risk of type 2 diabetes. BMC Public Health. (2010)
- Faghihi T, et al. A randomized, placebo-controlled trial of selenium supplementation in patients with type 2 diabetes: effects on glucose homeostasis, oxidative stress, and lipid profile. Am J Ther. (2014)
- MacFarquhar JK, et al. Acute selenium toxicity associated with a dietary supplement. Arch Intern Med. (2010)
- Morris JS, Crane SB. Selenium toxicity from a misformulated dietary supplement, adverse health effects, and the temporal response in the nail biologic monitor. Nutrients. (2013)
- Prevost N, English JC 3rd. Xanthotrichia (yellow hair) due to selenium sulfide and dihydroxyacetone. J Drugs Dermatol. (2008)
(Common misspellings for Selenium include selenum, selenim, selinium, selinim, selenyum)