Definition: Selenium is a cofactor for glutathione peroxidase, and selenium functions as an antioxidant. Selenium also plays a role in the conversion of thyroxine to triiodothyronine. In addition, selenium enhances immune function and has antiviral activity.

  • In animals, manifestations of selenium deficiency include hair loss, growth retardation, infertility, anemia, and pancreatic atrophy.
  • Vitamin E deficiency appears to exacerbate the effects of selenium deficiency. In animals, combined deficiency of these nutrients has resulted in pathologic lesions of the heart, skeletal muscle, and liver, and sudden death.
  • In humans, dietary selenium deficiency (possibly in combination with a viral infection) was implicated as a major contributing factor to Keshan disease, an endemic cardiomyopathy that affected children in China. When children in endemic areas began receiving selenium supplements in the 1970s, the incidence of this disease fell dramatically.
  • Selenium deficiency secondary to long-term administration of selenium-free total parenteral nutrition has resulted in cardiomyopathy, muscle pain, and weakness, elevations of liver enzymes, and white fingernail beds.
  • The levels and chemical forms of selenium in plant-based foods vary according to the composition and selenium content of soil in which the plants are grown. Selenium-rich food sources include Brazil nuts, grains, seafood, organ meats, poultry, and dairy products.
  • Selenium is among the most toxic of the essential minerals. Adverse effects of excessive selenium intake include hair loss, brittleness or loss of the nails, white spots on the nails, dermatitis, lassitude, depression, and neurological abnormalities (including peripheral anesthesia, acropares-thesia, pain in the extremities, convulsions, and in severe cases numbness, convulsions, and paralysis). Death has occurred in cases of extreme selenium poisoning.

Drug interactions

  • Selenium supplementation has been reported to decrease the number of side effects of cancer chemotherapy, including nephrotoxicity, bone marrow suppression, leukopenia, infections, hair loss, gastrointestinal symptoms, and muscle damage.

Nutrient interactions

  • Vitamin C: Vitamin C appears to convert sodium selenite to elemental selenium, making it unavailable for absorption.
  • Vitamin E: Selenium deficiency appears to aggravate the effects of vitamin E deficiency in animals. In addition, administration of vitamin E prevented some of the manifestations of selenium toxicity in mice.
  • In people who are severely deficient in iodine, selenium supplementation can trigger or exacerbate hypothyroidism, apparently by increasing the metabolism of thyroxine by the selenoenzyme, type 1 iodothyronine 5′-deiodinase.

Based on these findings, in patients at risk for severe iodine deficiency, iodine deficiency should be identified and corrected before supplementing with selenium. It would also be prudent to administer iodine to patients receiving selenium who are at risk for mild-to-moderate iodine deficiency.

  • Polyunsaturated fatty acids. Studies in animals and humans have shown that ingesting large amounts of omega-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid) increases the requirement for selenium.
  • Zinc and copper. Administration of very large amounts of zinc (4,000 mg/kg of diet) or copper (1,600 mg/kg of diet) induced selenium deficiency in rats. These findings raise the possibility that supplementation with more moderate amounts of zinc or copper would increase selenium requirements.


  • A number of different selenium preparations are available, including sodium selenite, sodium selenate, selenomethionine, selenocysteine, and high-selenium yeast. None of these preparations has clearly been shown to be preferable to the others.

Dosage and administration

  • The dosage of selenium used in most clinical trials was 100–200 μg/day

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