甲基汞诱导小鼠胸腺细胞Ca2+依赖性超极化:使用荧光染料的流式细胞术研究

Yasuo Oyama, David O. Carpenter , Shinya Ueno , Hiromi Hayashi, Fukiyo Tomiyoshi
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引用次数: 25

摘要

用荧光染料检测了甲基汞对小鼠胸腺细胞的膜电位和细胞内Ca2+的影响。浓度为1 ωM或更高(高达30 ωM)的甲基汞以剂量依赖的方式产生超极化。肉毒杆菌毒素和奎宁,而不是4-氨基吡啶和四乙基铵,能显著抑制甲基汞诱导的超极化。去除外部Ca2+降低了超极化程度。在无Ca2+条件下,用A23187预处理胸腺细胞可消除甲基汞诱导的超极化。在正常和游离Ca2+条件下,甲基汞增加细胞内Ca2+浓度。结果表明,细胞内Ca2+的增加是通过细胞内储存的Ca2+释放以及外部Ca2+的内流介导的。因此,甲基汞可能会增加细胞内Ca2+浓度,导致小鼠胸腺细胞Ca2+依赖性K+电导的激活。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Methylmercury induces Ca2+-dependent hyperpolarization of mouse thymocytes: a flow cytometric study using fluorescent dyes

The effect of methylmercury on mouse thymocytes was examined using fluorescent dyes for membrane potential and intracellular Ca2+. Methylmercury at concentrations of 1 ωM or higher (up to 30 ωM) produced hyperpolarization in a dose-dependent fashion. Charybdotoxin and quinine, but not 4-aminopyridine and tetraethylammonium, greatly suppressed methylmercury-induced hyperpolarization. Removal of external Ca2+ reduced the degree of hyperpolarization. Pretreatment of thymocytes with A23187 under Ca2+-free conditions abolished the hyperpolarization induced by methylmercury. Under both normal and Ca2+-free conditions methylmercury increased the intracellular concentration of Ca2+. The results suggest that the increase in intracellular Ca2+ is mediated through a Ca2+ release from intracellular stores as well as through influx of external Ca2+. Therefore, it is likely that methylmercury increases the intracellular concentration of Ca2+, resulting in activation of Ca2+-dependent K+ conductance of mouse thymocytes.

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