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目的 为揭示镉损害的细胞分子学机制。方法 利用镉中毒性肾损伤动物模型和凝胶渗透层析技术 ,观察了镉性肾损害时胞浆中钙稳态的变化及其与肾损伤之间的关系。结果 随着隔作用时间的延长 ,肾皮质中尿蛋白 ,尿NAG不断升高。肾胞浆中总钙和非蛋白结合钙均显著升高 ,Ca2 + -Mg2 + -ATPase活性也相应升高。结论 镉性肾损害过程中 ,细胞钙稳态受到破坏 ,从而介导了肾功能的异常
Aim To reveal the cellular molecular mechanisms of cadmium damage. Methods The animal model of cadmium poisoning renal injury and gel permeation chromatography were used to observe the changes of calcium homeostasis in cadmium-induced renal damage and its relationship with renal injury. Results With the extension of septal time, urinary protein and urinary NAG in renal cortex continuously increased. The total calcium and non-protein bound calcium in renal cytoplasm were significantly increased, Ca2 + -Mg2 + -ATPase activity increased accordingly. Conclusions During the process of cadmium-induced renal damage, the calcium homeostasis is disrupted, which mediates renal dysfunction