A chloride dependent K+ flux induced by N-ethylmaleimide in genetically low K+ sheep and goat erythrocytes.
A chloride dependent K+ flux induced by N-ethylmaleimide in genetically low K+ sheep and goat erythrocytes.
复制标题
N-乙基马来酰亚胺在遗传性低 K 绵羊和山羊红细胞中诱导氯离子依赖性 K 通量。
DOI：
10.1016/0006-291x(80)90445-3
复制
发表时间：
1980
影响因子：
3.1
通讯作者：
B. E. Theg
中科院分区：
文献类型：
--
作者：
P. Lauf;B. E. Theg
通过示踪剂内流或净流出法测量，在遗传上低钾+而非高钾+的绵羊和山羊红细胞中，n -乙基马来酰亚胺诱导了瓦巴因不敏感的钾+通量。在Cl−或Br−介质中观察到K+通量增加，而在no3−、so4 2−和po4 2−介质中没有。n -乙基马来酰亚胺的作用不同于副氯苯甲苯甲酸酯或其磺酸衍生物，后者增加了K+和Na+在红细胞膜上的被动运动。n -乙基马来酰亚胺的瞬时选择性作用表明，巯基控制着K+ Cl−运输系统，该系统与低K+基因有关，在成年反刍动物红细胞中显然是功能沉默的。
In genetically low K+ but not in high K+ red cells of sheep and goat N-ethylmaleimide induced a ouabain insensitive K+ flux as measured by tracer influx or net efflux methods. The augmented K+ flux was observed in Cl− or Br− but not in NO 3−, SO 4 2− or PO 4 2− media. The action of N-ethylmaleimide was distinct from that of parachloromercuribenzoate or its sulfonic acid derivative which increased both passive K+ and Na+ movements across the red cell membrane. The instantaneous selective action of N-ethylmaleimide suggests that sulfhydryl groups control a K+ Cl− transport system which, associated with the low K+ gene, is apparently functionally silent in adult ruminant red cells.