Abstract
75SeO32− was found to be actively metabolized by bovine erythrocytes. Release of 75Se from red cells was inhibited by 20 mM arsenate, 1.3 mM chromate, 0.5 mM iodoacetamide, 1.0 mM p-chloromercuribenzoate, or high levels of selenite while 20 mM fluoride or 1.0 mM azide had no effect. None of these metabolic inhibitors affected red cell transport of 75SeO42− or 75Se-selenomethionine, which apparently occurred by diffusion. Dialysis of erythrocytes caused an increased uptake of 75SeO32− due to an impairment of 75Se efflux. This effect was prevented by dialysis against 14 mM glucose but not by the presence of 10 mM inosine and 1 mM adenine, the latter added to maintain ATP levels. A hypothesis is proposed to account for the experimental data describing erythrocyte uptake and metabolism of selenite and the likely selenocompound extruded from the cells.
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