Author:

Keywords:

Biological Transport, Active, Cadmium, Dose-Response Relationship, Drug, Erythrocyte Membrane, Humans, Male, Na(+)-K(+)-Exchanging ATPase, Potassium, Potassium Channels, Sodium, Sodium Channels, Science & Technology, Life Sciences & Biomedicine, Public, Environmental & Occupational Health, RED-BLOOD-CELLS, ADENOSINE-TRIPHOSPHATASE ACTIVITY, ESSENTIAL-HYPERTENSION, POTASSIUM-CHANNELS, SODIUM-TRANSPORT, DIVALENT METALS, LYMPHOCYTES, INHIBITION, EXCHANGER, FLUXES, Sodium-Potassium-Exchanging ATPase

Abstract:

The effects of cadmium (Cd2+) on Na+,K(+)-ATPase in disrupted human erythrocyte membranes and on various transmembrane Na+ and K+ transport systems in intact erythrocyte suspensions were studied. Cadmium2+ inhibited the erythrocyte Na+,K(+)-ATPase enzyme with a 50% inhibition at a Cd2+ concentration of 6.25 microM. The Cd2+ inhibition in the human erythrocyte was non-competitive with respect to Na+,K+, and ATP. Cadmium2+ exerted no acute effect, however, on the Na+,K(+)-ATPase pump activity as measured by the ouabain sensitive 86Rb uptake or Na+ efflux in intact red blood cells. Cadmium2+ also inhibited the Ca2+ dependent K+ channels in human red blood cells, whereas it had no effect on Na+,K+ cotransport, Na+,Li+ countertransport, anion carrier, and the number of active Na+ pump units. The data indicate that in human erythrocytes under acute conditions Cd2+ exerts an inhibitory effect on Na+,K(+)-ATPase enzyme in disrupted erythrocytes and the Ca2+ stimulated K+ efflux in intact red blood cells without affecting the Na+ pump, Na+,K+ cotransport, and Na+,Li+ countertransport activity.