摘要
通过观察肾小管上皮细胞内Ｎａ＋－Ｋ＋－ＡＴＰ酶活性、胞浆游离钙离子浓度及超微结构的变化，系统研究了重金属镉致肾小管细胞损伤的发病机理。结果表明，镉染毒后，肾小管上皮细胞内Ｎａ＋－Ｋ＋－ＡＴＰ酶活性明显受抑，抑制率为８２．４％，胞浆游离钙离子浓度较对照组明显增加（Ｐ＜０．０１），且伴有一系列超微结构损害。提示，镉致肾损伤时肾小管上皮细胞内Ｎａ＋－Ｋ＋－ＡＴＰ酶活性受抑与胞浆游离钙离子浓度增加有明显的相关关系，胞内钙稳态失衡可能是镉致肾小管损伤的重要因素之一。
he mechanism of effects of cadmium on rabbit renal proximal tubule epithelial
cells were studied by measuring Na+-K+-ATPase activity and cytosolic free calcium and by
observing ultrastructural change of cells. After incubation with Cd,Na+-K+-ATPase activity of
proxinal tubule epithelial cells was significantly suppressed. The rate of suppression was
82.4%. At the sametime,cyttoslic free calcium concentration was increased as comparted
control(367.1±28.6nmol/L vs 2316±18. 3nmol/L, P<0.01)and ultrastructral damage of ce11s
were shwed.The study suggested that there a relationship between suppressing of
Na+-K+-ATPase activity and increasing of cytosolic free calcium,and that imbalance of calcium
homeostasis is an important factorof proximal tubule cells injury caused by cadmium.
出处
《中华劳动卫生职业病杂志》
CAS
CSCD
1995年第2期75-77,共3页
Chinese Journal of Industrial Hygiene and Occupational Diseases
基金
国家自然科学基金
关键词
镉
毒性
肾小管
上皮细胞
钙稳态
ATP酶
Na+-K+-ATPase Cadmium Renal tubule epithelial cells Calcium homeostasis
