弱磁场对骨骼肌肌质网钙调控作用的研究

Effects of Weak Magnetic Field on Ca^(2+)Modulation of Skeletal Muscle Sarcoplamic Reticulum

目的:探讨弱磁场对提取的骨骼肌肌质网系(SR)Ca^(2+)转运、钙泵(Ca^(2+)-Mg^(2+)-ATPase)及钙释放通道(RyR)活性的影响,从分子水平和细胞信号系统的角度来解释生物电磁效应。方法:利用动态光谱法检测0.4 mT弱磁场辐照过的SR Ca^(2+)转运、Ca^(2+)-ATPase活性,还原型辅酶(NADH)的氧化初速率和超氧(O_2^-)产率,以及用同位素标记方法检测[~3H]-Ryanodine与RyR的平衡结合度。结果:弱磁场辐照引起SR的Ca^(2+)摄取功能和Ca^(2+)-ATPase的活性明显下降,Ca^(2+)释放和[~3H]-Ryanodine平衡结合度上升,同时上调了NADH的氧化初速率和O_2^-的产率。结论:提示0.4 mT弱磁场辐照30 min对SR Ca^(2+)-ATPase活性有明显抑制,对RyR有一定的激活效果。

Objective：Discuss the effects of weak magnetic field on isolated sarcoplasmic reticulum（SR） Ca（2＋） modulation, calcium pump（Ca（2＋）-Mg（2＋）-ATPase） and Ca（2＋） release channel（Ryanodine Receptor,RyR） activity,so as to explain the mechanism of biological effects caused by electromagnetic fields in terms of molecular level and signal transduction system.Methods：The Ca（2＋） modulation and Ca（2＋）-ATPase activity,NADH oxidation initial rates and superoxide production of SR exposed to 0.4 mT weak magnetic field（MF） were investigated with dynamic Ca（2＋） dye spectrum method, [3H]-Ryanodine binding assay was investigated by isotope Labeling.Results：Weak MF exposure decreased SR Ca（2＋） uptake and Ca（2＋）-ATPase activity obviously,increased SR Ca（2＋） release and[3H]-Rryanodine binding,up-regulated the initial rates of NADH oxidation and the production of superoxide.Conclusion：It is indicated that 0.4 mT weak magnetic field exposure for 30 min inhibited Ca（2＋）-ATPase activity and promoted the RyR channel function.