Negendank W, Shaller C
J Cell Physiol. 1982 Mar;110(3):291-9. doi: 10.1002/jcp.1041100312.
Lymphocytes depleted of ATP by incubation in iodoacetate (IAA) and nitrogen (N2) lost K and gained Na. Isotopic Na exchange showed a fast fraction and a slower exponential fraction, the latter conventionally assumed to reflect surface membrane properties. The gain of cell Na was not accounted for by a decrease in 22Na efflux in either the slow or the fast fraction. After 3-5 hours, Na efflux increased. These results led us to question the concept that normal cell ion levels are maintained by an ATPase pump and could not be explained by exchange diffusion, co-transport, countertransport, or other inherently dissipative mechanisms. The data are, on the other hand, consistent with the concept that cell ion contents are determined by their relative exclusion from cell water coupled with selective adsorption onto fixed macromolecular anionic sites within the cell. In this view, the IAA,N2-induced rise in cell Na is due to the occupancy of adsorption sites losing K, while the increased isotopic exchange is due to a decreased activation energy for ion-site interaction.
通过在碘乙酸盐（IAA）和氮气（N₂）中孵育而耗尽ATP的淋巴细胞失去了钾并获得了钠。同位素钠交换显示出一个快速部分和一个较慢的指数部分，传统上认为后者反映了表面膜的特性。细胞钠的增加在慢速或快速部分中均不能用²²Na外流的减少来解释。3 - 5小时后，钠外流增加。这些结果使我们质疑正常细胞离子水平由ATP酶泵维持且无法用交换扩散、协同转运、逆向转运或其他固有耗散机制来解释的概念。另一方面，这些数据与细胞离子含量由其相对排除于细胞水之外以及与细胞内固定大分子阴离子位点的选择性吸附相结合来决定的概念一致。按照这种观点，IAA、N₂诱导的细胞钠升高是由于失去钾的吸附位点被占据，而同位素交换增加是由于离子 - 位点相互作用的活化能降低。
