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维生素E补充剂对大鼠实验性糖尿病中糖尿病诱导的氧化应激的影响。

Effect of vitamin E supplementation on diabetes induced oxidative stress in experimental diabetes in rats.

作者信息

Garg Madhu C, Chaudhary Dharam P, Bansal Devi D

机构信息

Department of Biochemistry, Panjab University, Chandigarh, India.

出版信息

Indian J Exp Biol. 2005 Feb;43(2):177-80.

PMID:15782820
Abstract

Diabetes induced by streptozotocin (50 mg/kg body wt, i.p.) in the rats substantially increased the plasma glucose and malondialdehyde levels along with corresponding decrease in the antioxidants levels. Supplementation of vitamin E (200 mg/kg body wt., ip) for 5 weeks resulted in non-significant decrease in the blood glucose levels but plasma malondialdehyde levels were reduced to below normal levels. Plasma vitamin E, vitamin C, uric acid and red blood cell glutathione levels were also restored to near normal levels on vitamin E supplementation to diabetic rats as compared to control (diabetic) rats. The activities of antioxidant enzymes, catalase (EC 1.11.1.6), glutathione peroxidase (GSHPx EC 1.11.1.9), and glutathione reductase (GR EC 1.6.4.2) were also concomitantly restored to near normal levels by vitamin E supplementation to diabetic rats. The results clearly demonstrated that vitamin E supplementation augments the antioxidant defense mechanism in diabetes and provides evidence that vitamin E may have a therapeutic role in free radical mediated diseases.

摘要

链脲佐菌素(50毫克/千克体重,腹腔注射)诱导的大鼠糖尿病显著提高了血浆葡萄糖和丙二醛水平,同时抗氧化剂水平相应降低。连续5周补充维生素E(200毫克/千克体重,腹腔注射)导致血糖水平无显著下降,但血浆丙二醛水平降至正常水平以下。与对照(糖尿病)大鼠相比,给糖尿病大鼠补充维生素E后,血浆维生素E、维生素C、尿酸和红细胞谷胱甘肽水平也恢复到接近正常水平。糖尿病大鼠补充维生素E后,抗氧化酶过氧化氢酶(EC 1.11.1.6)、谷胱甘肽过氧化物酶(GSHPx EC 1.11.1.9)和谷胱甘肽还原酶(GR EC 1.6.4.2)的活性也随之恢复到接近正常水平。结果清楚地表明,补充维生素E可增强糖尿病中的抗氧化防御机制,并提供证据表明维生素E可能在自由基介导的疾病中具有治疗作用。

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