钙超载与氧自由基：镉致离体肾小管上皮细胞损伤中的作用及联系

钙超载与氧自由基机制是细胞发生损伤的两大重要分子学机制。本文以离体肾小管上皮细胞为研究对象，重金属隔为损伤因素，着重探讨了镉致肾小管损伤中钙超载及氧自由基双重损伤机制的各自作用及联系，此外，尚观察了中药三七皂甙对上述机制的可能影响。结果发现，当镉与肾小管上皮细胞共同孵育后，［Ｃａ＾＋＋］ｉ及脂质过氧化代谢产物明显升高，氧自由基清除酶活力下降，提示钙超载机制及氧自由基机制共同参与了镉致肾小管上皮细胞

REACTIVE OXYGEN SPECIES AND CALCIUMOVERLOAD:EFFECT ON PROXIMAL TUBULECELLS iN CADMIUM CONDITION

he effect of two important factors,calcium over-load and ROS, of proximal tubule epithelial cell injurywere assessed by measuring cytosolic free calcium,content of products of lipid peroxidation, activity ofSOD,CAT,and observating ultrastructure change ofcells.A Chinese medicine, panax notoginseng(PNS),was also used to vertify the possibility of above mecha-nism.These studies suggested that calcium overloadand ROS are the factors of proximal tubular cells in-jury and can influence,and stimulate each other.Panax Notoginseng can affect ROS system by blockingcalcium passage,and safeguarding proximal tubulecells from injury caused by cadmium.