Jungwirth A, Paulmichl M, Lang F
Institute for Physiology, University of Innsbruck, Austria.
Kidney Int. 1990 Jun;37(6):1477-86. doi: 10.1038/ki.1990.138.
The kidney is a main target organ for cadmium toxicity. The present study has been performed to test for effects of cadmium on electrical properties of cultured subconfluent kidney (MDCK) cells. Cadmium leads to a rapid, sustained and reversible hyperpolarization of the cell membrane, paralleled by an increase of the potassium selectivity and a decrease of the resistance. Thus, cadmium increases the potassium conductance of the cell membrane. The half maximal effect is elicited congruent to 0.2 microM, a concentration encountered during chronic cadmium intoxication. At extracellular calcium concentration reduced to less than 0.1 microM, 5 microM cadmium leads to a transient hyperpolarization, which can be elicited only once. High concentrations (50 microM) of cadmium lead to a sustained hyperpolarization even at extracellular calcium concentrations of less than 0.1 microM. According to fluorescence measurements cadmium leads to an increase of intracellular calcium activity, which is sustained at 1 mM and transient at less than 1 microM extracellular calcium activity. In conclusion, cadmium at low concentrations enhances the potassium conductance in a calcium dependent way. The observations suggest that cadmium enhances intracellular calcium both by recruitment from intracellular stores and by modification of calcium transport across the cell membrane. At high concentrations cadmium enhances the potassium conductance independently from enhanced intracellular calcium activity.
肾脏是镉毒性作用的主要靶器官。本研究旨在检测镉对培养的亚汇合肾（MDCK）细胞电特性的影响。镉可导致细胞膜快速、持续且可逆的超极化，同时钾选择性增加而电阻降低。因此，镉增加了细胞膜的钾电导。半数最大效应在约0.2微摩尔时出现，这是慢性镉中毒时会遇到的浓度。在细胞外钙浓度降至低于0.1微摩尔时，5微摩尔镉会导致短暂的超极化，且只能引发一次。即使在细胞外钙浓度低于0.1微摩尔时，高浓度（50微摩尔）的镉也会导致持续的超极化。根据荧光测量，镉会导致细胞内钙活性增加，在细胞外钙活性为1毫摩尔时保持持续增加，而在低于1微摩尔时为短暂增加。总之，低浓度的镉以钙依赖的方式增强钾电导。这些观察结果表明，镉通过从细胞内储存库募集以及改变跨细胞膜的钙转运来增强细胞内钙。在高浓度时，镉独立于增强的细胞内钙活性增强钾电导。
