Evcimen N D, Pekiner B D, Nebioglu S
Department of Biochemistry, University of Ankara, Faculty of Pharmacy, Turkey.
Diabetes Metab. 1999 Nov;25(5):399-403.
Kidney Ca(2+)-ATPase activity was altered in streptozotocin (STZ)-induced diabetic rats. Male rats, 200-250 g, were rendered diabetic by injection of STZ 45 mg/kg body weight via the tail vein. Following injection, control rats and diabetic rats at 1, 4, 8 or 15 weeks were sacrificed. Kidney tissues were obtained for the isolation of Ca(2+)-ATPase. Ca(2+)-ATPase activity was determined spectrophotometrically. Total calcium was measured by atomic absorption spectrophotometry. Diabetic rats had significantly elevated blood glucose levels compared to controls. Blood glucose levels were 92.92 +/- 1.215 mg/dl (mean +/- S.E.M.) for the control group, and 362.50 +/- 9.613 mg/dl at one week and > 500 mg/dl at 4, 8 and 15 weeks of diabetes. Enzyme activities were significantly higher at 4, 8 and 15 weeks of diabetes than in the control group (p < 0.001). There was no significant increase at one week of diabetes. Ca(2+)-ATPase activity was 0.43 +/- 0.003 U/L, 0.517 +/- 0.058 U/L, 0.707 +/- 0.078 U/L, 0.730 +/- 0.006 U/L and 0.715 +/- 0.055 U/L respectively for controls and rats at 1, 4, 8 and 15 weeks of diabetes. Calcium levels in diabetic rat kidneys were also significantly higher than for controls. The increase in enzyme activity may have been caused by higher calcium levels in diabetic kidneys resulting from a compensatory response of the enzyme to high levels of the ion.
链脲佐菌素(STZ)诱导的糖尿病大鼠肾脏钙(Ca2+)-ATP酶活性发生改变。选用体重200 - 250 g的雄性大鼠,通过尾静脉注射45 mg/kg体重的STZ使其患糖尿病。注射后,在1、4、8或15周处死对照大鼠和糖尿病大鼠。获取肾脏组织用于分离钙(Ca2+)-ATP酶。采用分光光度法测定钙(Ca2+)-ATP酶活性。通过原子吸收分光光度法测量总钙含量。与对照组相比,糖尿病大鼠的血糖水平显著升高。对照组血糖水平为92.92±1.215 mg/dl(平均值±标准误),糖尿病1周时为362.50±9.613 mg/dl,糖尿病4、8和15周时>500 mg/dl。糖尿病4、8和15周时酶活性显著高于对照组(p<0.001)。糖尿病1周时无显著升高。对照组及糖尿病1、4、8和15周大鼠的钙(Ca2+)-ATP酶活性分别为0.43±0.003 U/L、0.517±0.058 U/L、0.707±0.078 U/L、0.730±0.006 U/L和0.715±0.055 U/L。糖尿病大鼠肾脏中的钙水平也显著高于对照组。酶活性的增加可能是由于糖尿病肾脏中较高的钙水平导致,这是该酶对高水平离子的一种代偿反应。