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艾氏腹水癌细胞中 Na+、K+ 和 Cl- 的电沉默协同转运

Electrically silent cotransport on Na+, K+ and Cl- in Ehrlich cells.

作者信息

Geck P, Pietrzyk C, Burckhardt B C, Pfeiffer B, Heinz E

出版信息

Biochim Biophys Acta. 1980 Aug 4;600(2):432-47. doi: 10.1016/0005-2736(80)90446-0.

Abstract

A cotransport system for Na+, K+ and Cl- in Ehrlich cells is described. It is insensitive towards ouabain but specifically inhibited by furosemide and other 'high ceiling' diuretics at concentrations which do not affect other pathways of the ions concerned. As the furosemide-sensitive fluxes of these ions are no affected by changes in membrane potential, and as their complete inhibition by furosemide does not appreciably alter the membrane potential, they appear to be electrically silent. Application of the pulse-response methods in terms of irreversible thermodynamics reveals tight coupling between the furosemide-sensitive flows of Na+, K+ and Cl- (q close to unity for all three combinations) at a stoichiometry of 1: 1 : 2. The site for each of the ions appears to be rather specific: K+ can be replaced by Rb+ but not by other cations tested whereas Cl- can be poorly replaced by Br- but not by NO(-)3, in contradistinction to the Cl(-)-OH- exchange system. The cotransport system appears to function in cell volume regulatin as it tends to make the cell swell, thus counteracting the shrinking effect of the ouabain-sensitive (Na+, K+) pump. The experiments presented could not clarify whether the cotransport process is a primary or secondary active one; while incongruence between transport and conjugated driving force seems to indicate primary active transport, it is very unlikely that hydrolysis of ATP supplies energy for the transport process, since thre is not stimulation of ATP turnover observable under operation of the cotransport system.

摘要

本文描述了艾氏腹水癌细胞中Na+、K+和Cl-的协同转运系统。该系统对哇巴因不敏感,但可被呋塞米和其他“高效能”利尿剂特异性抑制,且抑制浓度不影响相关离子的其他转运途径。由于这些离子对呋塞米敏感的通量不受膜电位变化的影响,且呋塞米对其完全抑制不会明显改变膜电位,因此它们似乎是电中性的。应用不可逆热力学的脉冲响应方法表明,呋塞米敏感的Na+、K+和Cl-流之间紧密偶联(三种组合的q均接近1),化学计量比为1:1:2。每种离子的结合位点似乎具有相当的特异性:K+可被Rb+取代,但不能被其他测试阳离子取代;而Cl-可被Br-部分取代,但不能被NO3-取代,这与Cl--OH-交换系统不同。该协同转运系统似乎在细胞体积调节中发挥作用,因为它倾向于使细胞肿胀,从而抵消哇巴因敏感的(Na+,K+)泵的收缩作用。本文所做的实验无法阐明协同转运过程是原发性主动转运还是继发性主动转运;虽然转运与共轭驱动力之间的不一致似乎表明是原发性主动转运,但ATP水解为转运过程提供能量的可能性极小,因为在协同转运系统运行时未观察到ATP周转的刺激。

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