Abstract
The effect of sodium selenite on DNA and sulfated proteoglycan synthesis by cultured rabbit articular and growth plate chondrocytes was studied as an in vitro model for Kashin-Beck disease. The selenium content of a defined medium (DMEM, fibroblast growth factor, insulin, and dexamethasone) was below the limit of detection by isotope dilution mass spectrometry. The chondrocytes were viable in the Se-free basal medium. Selenite over a range of 5 X 10(-9) M to 5 X 10(-7) M had no stimulatory effect on DNA or sulfated proteoglycan synthesis by either type of chondrocyte or skin fibroblasts. Proliferation of bovine endothelial cells was enhanced by 5 X 10(-7) M Se. At Se concentrations of greater than or equal to 10(-6) M, there was progressive inhibition of cell growth and radiosulfate incorporation of the connective tissue cells; bovine endothelial cells were more resistant. Twice equimolar concentrations of vitamins C and E exerted no protective effect against the cytotoxicity of higher concentrations of Se. Se supplementation also failed to stimulate growth of human infant chondrocytes. The model enabled simulation of conditions of hyposelenosis below those encountered in nature. The data provide no evidence that chondrocytes have idiosyncratic requirements for Se, and do not support the hypothesis that Se deficiency is a major etiologic factor in Kashin-Beck disease.
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