Selenium deficiency decreases antioxidative capacity and is detrimental to bone microarchitecture in mice.

Selenium (Se), an essential mineral, plays a major role in cellular redox status and may have beneficial effects on bone health. The objective of this study was to determine whether Se deficiency affects redox status and bone microarchitecture in a mouse model. Thirty-three male C57BL/6J mice, 18 wk old, were randomly assigned to 3 groups. Mice were fed either a purified, Se-deficient diet (SeDef) containing ∼0.9 μg Se/kg diet, or Se-adequate diets containing ∼100 μg Se/kg diet from either selenomethionine (SeMet) or pinto beans (SeBean) for 4 mo. The Se concentration, glutathione peroxidase (GPx1) activity, and GPx1 mRNA in liver were lower in the SeDef group than in the SeMet or SeBean group. The femoral trabecular bone volume/total volume and trabecular number were less, whereas trabecular separation was greater, in the SeDef group than in either the SeMet or SeBean group (P < 0.05). Bone structural parameters between the SeMet and SeBean groups did not differ. Furthermore, Serum concentrations of C-reactive protein, tartrate-resistant acid phosphatase, and intact parathyroid hormone were higher in the SeDef group than in the other 2 groups. These findings demonstrate that Se deficiency is detrimental to bone microarchitecture by increasing bone resorption, possibly through decreasing antioxidative potential.