目的: 探讨弱磁场对提取的骨骼肌肌质网系(SR)Ca2+转运、钙泵(Ca2+-Mg2+-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 Ca2+转运、Ca2+-ATPase活性, 还原型辅酶(NADH)的氧化初速率和超氧(O2-·)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Ca2+摄取功能和Ca2+-ATPase的活性明显下降, Ca2+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O2-·的产率。 结论: 提示0.4 mT弱磁场辐照30 min对SR Ca2+-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) Ca2+ modulation, calcium pump (Ca2+-Mg2+-ATPase) and Ca2+ 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 Ca2+ modulation and Ca2+-ATPase activity, NADH oxidation initial rates and superoxide production of SR exposed to 0.4 mT weak magnetic field (MF) were investigated with dynamic Ca2+ dye spectrum method, ［3H］-Ryanodine binding assay was investigated by isotope Labeling. Results: Weak MF exposure decreased SR Ca2+ uptake and Ca2+-ATPase activity obviously, increased SR Ca2+ 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 Ca2+-ATPase activity and promoted the RyR channel function.