Oyama Y, Carpenter D O, Ueno S, Hayashi H, Tomiyoshi F
Laboratory of Cell Signaling Pharmacology, Graduate School of Human and Natural Environments, University of Tokushima, Japan.
Eur J Pharmacol. 1995 Jul 1;293(2):101-7. doi: 10.1016/0926-6917(95)00003-8.
The effect of methylmercury on mouse thymocytes was examined using fluorescent dyes for membrane potential and intracellular Ca2+. Methylmercury at concentrations of 1 microM or higher (up to 30 microM) 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 Ca(2+)-free conditions abolished the hyperpolarization induced by methylmercury. Under both normal and Ca(2+)-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 Ca(2+)-dependent K+ conductance of mouse thymocytes.
利用用于膜电位和细胞内Ca2+的荧光染料，研究了甲基汞对小鼠胸腺细胞的影响。浓度为1微摩尔或更高（最高30微摩尔）的甲基汞以剂量依赖的方式产生超极化。大蝎毒素和奎宁能极大地抑制甲基汞诱导的超极化，而4-氨基吡啶和四乙铵则不能。去除细胞外Ca2+可降低超极化程度。在无Ca(2+)条件下用A23187预处理胸腺细胞可消除甲基汞诱导的超极化。在正常和无Ca(2+)条件下，甲基汞均增加细胞内Ca2+浓度。结果表明，细胞内Ca2+的增加是通过细胞内储存库释放Ca2+以及细胞外Ca2+内流介导的。因此，甲基汞可能增加细胞内Ca2+浓度，导致小鼠胸腺细胞Ca(2+)依赖性钾电导激活。
