Author:
Jenkins K. J.,Hidiroglou M.
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.
Publisher
Canadian Science Publishing
Subject
Physiology (medical),Pharmacology,General Medicine,Physiology
Cited by
31 articles.
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