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首页> 外文期刊>Cell biology international. >Enhancing effects of diethyldithiocarbamate on increase of sodium channel by sulfur dioxide derivatives in ventricular myocytes.
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Enhancing effects of diethyldithiocarbamate on increase of sodium channel by sulfur dioxide derivatives in ventricular myocytes.

机译:二乙基二硫代氨基甲酸酯对心室肌细胞中二氧化硫衍生物增加钠通道的作用。

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The enhancing effects of diethyldithiocarbamate (DDC) on increase of sodium channel by sulfur dioxide derivatives in ventricular myocytes were studied using the whole cell patch-clamp technique to probe the mechanism of SO2 on the cardiovascular system in this study. Firstly, the effects of DDC and/or sulfur dioxide (SO2) derivatives on the activities of superoxide dismutase (SOD) were studied. The results showed that DDC decreased SOD activities significantly and SO2 derivatives had no significant effect on SOD activities; however, DDC and SO2 derivatives combined led to a significant decrease of SOD activities. In the electrophysiological test, DDC (1-100 mM) increased sodium current (INa) in a concentration-dependent manner and the concentration for half-maximum increase (EC50) was 20 mM. Addition of 20 mM DDC to the SO2 derivatives-containing medium significantly shifted the voltage-dependent activation curve of INa toward the hyperpolarizing direction (Vh are -51 mV, -53 mV and -54 mV, respectively) and shifted the steady-state inactivation curve to more positive potentials (Vh are -74 mV, -71 mV and -65 mV, respectively) compared with the control and 10 microM SO2 derivatives exposure. These results indicated that DDC could enhance the increasing effects on Na+ channels induced by SO2 derivatives, and suggested that the toxicity of SO2 on ventricular myocytes of rats was realized by free radical, especially O2-.
机译:利用全细胞膜片钳技术研究了二乙基二硫代氨基甲酸酯(DDC)对心室肌细胞中二氧化硫衍生物钠通道增加的增强作用,以探讨SO2对心血管系统的作用机制。首先,研究了DDC和/或二氧化硫(SO2)衍生物对超氧化物歧化酶(SOD)活性的影响。结果表明,DDC显着降低了SOD活性,SO2衍生物对SOD活性无明显影响。然而,DDC和SO2衍生物的结合导致SOD活性显着下降。在电生理测试中,DDC(1-100 mM)以浓度依赖的方式增加钠电流(INa),半最大增加浓度(EC50)为20 mM。向含SO2衍生物的介质中添加20 mM DDC会使INa的电压依赖性激活曲线显着移向超极化方向(Vh分别为-51 mV,-53 mV和-54 mV),并转移了稳态失活与对照和10 microM SO2衍生物暴露相比,曲线具有更大的正电位(Vh分别为-74 mV,-71 mV和-65 mV)。这些结果表明DDC可以增强SO 2衍生物诱导的Na +通道的增加作用,并表明SO 2对大鼠心室肌细胞的毒性是通过自由基尤其是O 2-实现的。

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