Abstract
Selenium (Se) is an essential trace element for humans and animals, and several findings suggest that dietary Se intake may be necessary for bone health. Such findings may relate to roles of Se in antioxidant protection, enhanced immune surveillance and modulation of cell proliferation. Elucidation of the mechanisms by which Se supports these cellular processes can lead to a better understanding of the role of this nutrient in normal bone metabolism. This article reviews the current knowledge concerning the molecular functions of Se relevant to bone health.
Highlights
Selenium (Se) is an essential nutrient, being required at 0.1–0.2 ppm in animal diets, and with a recommended daily allowance of 55 μg/day for both men and women [1]
bone marrow stromal cells (BMSCs) cultured in the presence of low Se concentrations (5–10 nM) show reduced expression of glutathione peroxidases (GPXs), thioredoxin reductases (TRRs) and other selenoproteins, as well as the appearance of micronuclei indicative of chromosomal damage [18]
Selenium is an essential nutrient that appears to play a role in bone health
Summary
Selenium (Se) is an essential nutrient, being required at 0.1–0.2 ppm in animal diets, and with a recommended daily allowance of 55 μg/day for both men and women [1]. It plays critical roles in a variety of physiological processes as an essential constituent of some 25 selenoenzymes in which it is present as the selenoamino acid, selenocysteine, not found in other proteins [2,3]. Low Se intakes have been associated with increased risk to bone disease [5,7,9,10]. We summarize current knowledge of the effects of Se on bone and the underlying mechanisms
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