Lijnen P, Staessen J, Fagard R, Amery A
Department of Pathophysiology, University of Leuven, Belgium.
Br J Ind Med. 1991 Jun;48(6):392-8. doi: 10.1136/oem.48.6.392.
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.
研究了镉(Cd2+)对破碎的人红细胞膜中Na+,K(+)-ATP酶以及完整红细胞悬液中各种跨膜Na+和K+转运系统的影响。Cd2+抑制红细胞Na+,K(+)-ATP酶,在Cd2+浓度为6.25微摩尔时抑制率达50%。人红细胞中的Cd2+抑制作用对Na+、K+和ATP而言是非竞争性的。然而,通过哇巴因敏感的86Rb摄取或完整红细胞中的Na+流出所测得的Na+,K(+)-ATP酶泵活性,Cd2+并未产生急性影响。Cd2+还抑制人红细胞中Ca2+依赖性K+通道,而对Na+,K+协同转运、Na+,Li+逆向转运、阴离子载体以及活性Na+泵单位数量没有影响。数据表明,在急性条件下,Cd2+对破碎红细胞中的Na+,K(+)-ATP酶以及完整红细胞中Ca2+刺激的K+流出具有抑制作用,而不影响Na+泵、Na+,K+协同转运和Na+,Li+逆向转运活性。