Copper effects on ion transport across lamprey erythrocyte membrane:: Cl-/OH- exchange induced by cuprous ions
Copper effects on ion transport across lamprey erythrocyte membrane:: Cl-/OH- exchange induced by cuprous ions
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DOI：
10.1006/taap.1999.8736
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发表时间：
1999-09-15
影响因子：
3.8
通讯作者：
Nikinmaa, M
中科院分区：
文献类型：
--
作者：
Bogdanova, AY;Virkki, LV;Nikinmaa, M
我们研究了七鳃鳗红细胞的细胞体积，细胞内的pH值，和离子转运的预溶解铜浓度的影响。离子通量和pH值测定放射性示踪技术，膜片钳，火焰光度法。100 μ M的Prelytic CuSO 4浓度引起阴离子依赖性的细胞内酸化和增加Cl-流入后2分钟的滞后期。在抗坏血酸铜的存在下，放大的效果和滞后期被跳过。用N-苯基马来酰亚胺预处理细胞完全消除铜诱导的变化。铜处理引起的Na+通量在两个方向和净Na+吸收增加。铜诱导的Na+转运是部分阿米洛利（MIA）敏感的Na+/H+交换。铜激活Na+内流的阿米洛利不敏感部分的性质仍然未知。铜暴露15分钟后的细胞肿胀诱导调节性体积减少反应，涉及KCl通过K+和Cl-体积敏感性通道挤出。我们认为铜对离子转运的影响符合以下事件顺序：（i）二价铜离子在膜表面被还原成亚铜态，（ii）电中性对CuCl和CuOH介导氯离子/羟基交换，如之前对于三烷基锡所示，分散跨膜pH梯度，和（iii）细胞内pH的变化导致Na+/H+交换的激活，并且连续的体积变化引起RVD反应。(C)北京：科学出版社.
We studied the effects of prelytic copper concentrations on cell volume, intracellular pH, and ion transport in lamprey erythrocytes. Ion fluxes and pH were measured by radioactive tracer technique, patch clamp, and flame photometry. Prelytic CuSO4 concentration of 100 mu M caused anion-dependent intracellular acidification and increase in Cl- influx after 2 min lag-phase. In the presence of ascorbate copper effect was amplified and lag-phase was skipped. Pretreatment of the cells with N-phenyl maleimide abolished copper-induced changes completely. Copper treatment caused an increase in Na+ fluxes in both directions and a net Na+ uptake. Copper-induced Na+ transport was partially amiloride(MIA)-sensitive representing Na+/H+ exchange. The nature of the amiloride-insensitive fraction of copper-activated Na+ influx remains unknown. Cell swelling after 15 min of copper exposure induced regulatory volume decrease response involving KCI extrusion via K+ and Cl- volume-sensitive channels. We suggest that the effects of copper on ion transport fit the following sequence of events: (i) cupric ions are reduced to cuprous state on the membrane surface, (ii) electroneutral pairs CuCl and CuOH mediate chloride/hydroxyl exchange, as shown before for trialkyltin, dissipating transmembrane pH gradient, and (iii) changes in intracellular pH result in the activation of the Na+/H+ exchange and consecutive volume changes cause the RVD response. (C) 1999 Academic Press.