Selenium deficiency as a putative risk factor for osteoporosis

Abstract

The trace element selenium occurs in the soil in variable concentrations. Selenium is incorporated into proteins as selenocysteine, the 21st amino acid, by a complex translational mechanism. The human proteome comprises 25 yet only partly characterized selenoproteins which function as antioxidative scavengers, protein chaperones, thyroid hormone metabolising enzymes and selenium storing proteins. Antioxidative selenoenzymes (e.g. glutathione peroxidases and thioredoxin reductases) neutralize reactive oxygen species to avoid damage of the genome and proteome which otherwise would cause loss of cellular functions and induction of failsafe programs like apoptosis and senescence. Selenoproteins are important in bone metabolism as selenium deficiency is associated with osteopenia in animal models and with osteoarthropathy in humans. Selenoproteins are expressed in mesenchymal stem cells (MSC) and bone cells. The antioxidative capacity of MSC is restored and DNA damage is reduced by supplementing cells with selenite. The activity of plasma glutathione peroxidase and other antioxidative compounds is reduced in osteoporotic patients. The role of selenium dependent proteins in bone physiology and osteoporosis awaits further characterization. Population wide selenium supplementation in regions of low daily intake might optimize an individual's antioxidative capacity thereby ameliorating atherosclerosis, cancer incidence and possibly osteoporosis.