Kakkar R, Kalra J, Mantha S V, Prasad K
Department of Pathology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
Mol Cell Biochem. 1995 Oct 18;151(2):113-9. doi: 10.1007/BF01322333.
We hypothesized that oxygen free radicals (OFRs) may be involved in pathogenesis of diabetic complications. We therefore investigated the levels of lipid peroxidation by measuring thiobarbituric acid reactive substances (TBARS) and activity of antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT)] in tissues and blood of streptozotocin (STZ)-induced diabetic rats. The animals were divided into two groups: control and diabetic. After 10 weeks (wks) of diabetes the animals were sacrificed and liver, heart, pancreas, kidney and blood were collected for measurement of various biochemical parameters. Diabetes was associated with a significant increase in TBARS in pancreas, heart and blood. The activity of CAT increased in liver, heart and blood but decreased in kidney. GSH-Px activity increased in pancreas and kidney while SOD activity increased in liver, heart and pancreas. Our findings suggest that oxidative stress occurs in diabetic state and that oxidative damage to tissues may be a contributory factor in complications associated with diabetes.
我们推测氧自由基(OFRs)可能参与糖尿病并发症的发病机制。因此,我们通过测量链脲佐菌素(STZ)诱导的糖尿病大鼠组织和血液中的硫代巴比妥酸反应物质(TBARS)以及抗氧化酶[超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)]的活性,来研究脂质过氧化水平。将动物分为两组:对照组和糖尿病组。糖尿病10周后处死动物,收集肝脏、心脏、胰腺、肾脏和血液以测量各种生化参数。糖尿病与胰腺、心脏和血液中TBARS的显著增加有关。肝脏、心脏和血液中CAT的活性增加,但肾脏中CAT的活性降低。胰腺和肾脏中GSH-Px的活性增加,而肝脏、心脏和胰腺中SOD的活性增加。我们的研究结果表明,糖尿病状态下会发生氧化应激,组织的氧化损伤可能是糖尿病相关并发症的一个促成因素。