Ikehara T, Park K H, Yamaguchi H, Hosokawa K, Yoshizaki K, Miyamoto H, Aizawa K, Kinouchi Y
Department of Physiology, School of Medicine, The University of Tokushima, Tokushima, Japan.
Bioelectromagnetics. 2000 Apr;21(3):228-37. doi: 10.1002/(sici)1521-186x(200004)21:3<228::aid-bem9>3.0.co;2-i.
Effects of a switched, time-varying 1.7 T magnetic field on Rb(+)(K+) uptake by HeLa S3 cells incubated in an isosmotic high K(+) medium were examined. The magnetic flux density was varied intermittently from 0.07-1.7 T at an interval of 3 s. K(+) uptake was activated by replacement of normal medium by high K(+) medium. A membrane-permeable Ca(2+) chelating agent (BAPTA-AM) and Ca(2+)-dependent K(+) channel inhibitors (quinine, charibdotoxin, and iberiotoxin) were found to reduce the Rb(+)(K+) uptake by about 30-40%. Uptake of K(+) that is sensitive to these drugs is possibly mediated by Ca(2+)-dependent K(+) channels. The intermittent magnetic field partly suppress ed the drug-sensitive K(+) uptake by about 30-40% (P < 0.05). To test the mechanism of inhibition by the magnetic fields, intracellular Ca(2+) concentration ([Ca(2+)]c) was measured using Fura 2-AM. When cells were placed in the high K(+) medium, [Ca(2+)]c increased to about 1.4 times the original level, but exposure to the magnetic fields completely suppressed the increase (P < 0.01). Addition of a Ca(2+) ionophore (ionomycin) to the high K(+) medium increased [Ca(2+)]c to the level of control cells, regardless of exposure to the magnetic field. But the inhibition of K(+) uptake by the magnetic fields was not restored by addition of ionomycin. Based on our previous results on magnetic field-induced changes in properties of the cell membrane, these results indicate that exposure to the magnetic fields partly suppresses K(+) influx, which may be mediated by Ca(2+)-dependent K(+) channels. The suppress ion of K(+) fluxes could relate to a change in electric properties of cell surface and an inhibition of Ca(2+) influx mediated by Ca(2+) channels of either the cell plasma membrane or the inner vesicular membrane of intracellular Ca(2+) stores.
研究了交变、时变的1.7 T磁场对在等渗高钾培养基中培养的HeLa S3细胞摄取Rb⁺(K⁺)的影响。磁通密度以3 s的间隔在0.07 - 1.7 T之间间歇性变化。用高钾培养基替代正常培养基可激活K⁺摄取。发现一种膜通透性Ca²⁺螯合剂（BAPTA - AM）和Ca²⁺依赖性K⁺通道抑制剂（奎宁、查利毒素和iberiotoxin）可使Rb⁺(K⁺)摄取减少约30 - 40%。对这些药物敏感的K⁺摄取可能由Ca²⁺依赖性K⁺通道介导。间歇性磁场部分抑制了药物敏感的K⁺摄取，约为30 - 40%（P < 0.05）。为了测试磁场的抑制机制，使用Fura 2 - AM测量细胞内Ca²⁺浓度（[Ca²⁺]c）。当细胞置于高钾培养基中时，[Ca²⁺]c增加到约为原始水平的1.4倍，但暴露于磁场可完全抑制这种增加（P < 0.01）。向高钾培养基中添加Ca²⁺离子载体（ionomycin）可使[Ca²⁺]c增加到对照细胞的水平，无论是否暴露于磁场。但添加ionomycin并未恢复磁场对K⁺摄取的抑制作用。基于我们之前关于磁场诱导细胞膜特性变化的结果，这些结果表明暴露于磁场部分抑制了K⁺内流，这可能由Ca²⁺依赖性K⁺通道介导。K⁺通量的抑制可能与细胞表面电特性的变化以及对细胞质膜或细胞内Ca²⁺储存泡内膜的Ca²⁺通道介导的Ca²⁺内流的抑制有关。
