Determination of Ca2+-atpase activity in streptozotocin-induced diabetic rat liver.

Determination of Ca2+-atpase activity in streptozotocin-induced diabetic rat liver.
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链脲佐菌素诱导的糖尿病大鼠肝脏中 Ca2-atpase 活性的测定。

DOI:
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发表时间:
2002
期刊:
Diabetes, Nutrition and Metabolism. Clinical and Experimental
影响因子:
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通讯作者:
S. Nebioğlu
S. Nebioğlu
中科院分区:
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文献类型:
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作者:
B. Pekiner;E. N. Das;S. Nebioğlu

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研究了对照组和链脲佐菌素(STZ)诱导的糖尿病大鼠肝脏微粒体Ca2+- atp酶活性。雄性大鼠经尾静脉注射STZ (45 mg/kg体重)致糖尿病。分别处死1、4、8、10、15周的糖尿病大鼠和对照组大鼠。获得肝组织用于分离Ca2+- atp酶。用分光光度法测定Ca2+- atp酶活性,用荧光光度法测定肝组织中的脂质过氧化[以硫巴比妥酸反应物质(TBARS)测量]。用原子吸收分光光度法测定总钙。糖尿病动物在4、8、10和15周时的血糖水平为50 ~ 500 mg/dl。与对照组相比,糖尿病患者的所有周内Ca2+- atp酶活性均显著降低(p<0.001)。对照大鼠的Ca2+- atp酶活性为0.193 +/- 0.015 U/I,而糖尿病15周时的活性为0.130 +/- 0.015 U/I。与对照组相比,糖尿病大鼠肝脏钙水平差异无统计学意义。另一方面,糖尿病患者15周时TBARS升高67%。酶活性的降低可能是由肝组织中观察到的TBARS水平升高引起的,这表明脂质过氧化作用增加。
Microsomal Ca2+-ATPase activity was studied in control and streptozotocin (STZ)-induced diabetic rat livers. Male rats were rendered diabetic by injection of STZ (45 mg/kg body weight) via the tail vein. Diabetic rats at 1, 4, 8, 10 or 15 wk and control rats were sacrificed. Liver tissues were obtained for the isolation of Ca2+-ATPase. Ca2+-ATPase activity was determined spectrophotometrically and lipid peroxidation [measured as tiobarbituric acid reactive substances (TBARS)] in liver tissues was determined spectrofluorometrically. Total calcium was measured by atomic absorption spectrophotometry. Blood glucose levels of the diabetic animals were >500 mg/dl at 4, 8, 10 and 15 wk of diabetes. Ca2+-ATPase activity was significantly decreased at all weeks of diabetes compared to control group (p<0.001). Ca2+-ATPase activity of control rats was 0.193 +/- 0.015 U/I whereas activity was 0.130 +/- 0.015 U/I at 15 wk of diabetes. The difference in calcium levels of diabetic rat livers was not significantly different compared to control group. On the other hand TBARS were elevated by 67% at 15 wk of diabetes. The decrease in enzyme activity may have been caused by elevated TBARS levels observed in liver tissue sindicative of increased lipid peroxidation.