增强亚硫酸钠对急性分离大鼠海马 CA1 神经元钠电流的作用。
Enhancement of sodium metabisulfite on sodium currents in acutely isolated rat hippocampal CA1 neurons.
机构信息
Institute of Environmental Medicine and Toxicology, Research Center of Environmental Science and Engineering, Shanxi University, Taiyuan 030006, China.
出版信息
Environ Toxicol Pharmacol. 2005 Jul;20(1):35-41. doi: 10.1016/j.etap.2004.10.003. Epub 2004 Dec 8.
The effect of sodium metabisulfite (SMB) on voltage-gated sodium channel currents (I(Na)) was examined in freshly isolated rat hippocampal CA1 neurons using whole-cell patch-clamp technique under voltage-clamp conditions. SMB irreversibly enhanced I(Na) in a concentration-dependent manner, shifted the inactivation curve to more positive potential, without affecting the current activation curve. In addition, SMB increased the time to peak and the inactivation time constant of I(Na). Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) could all partly inhibit the effect of SMB on the sodium current. These results suggested that SMB have neuronal toxicity by increasing the excitability of neurons and its mechanism might involve the oxidative damage on ion channels.
亚硫酸钠（SMB）对电压门控钠离子通道电流（I(Na)）的影响，采用全细胞膜片钳技术在电压钳条件下，在新鲜分离的大鼠海马 CA1 神经元中进行了检测。SMB 以浓度依赖性的方式不可逆地增强 I(Na)，使失活曲线向更正的电位移动，而不影响电流激活曲线。此外，SMB 增加了 I(Na)的峰值时间和失活时间常数。超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx）都可以部分抑制 SMB 对钠电流的作用。这些结果表明，SMB 通过增加神经元的兴奋性产生神经元毒性，其机制可能涉及对离子通道的氧化损伤。
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