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J Diabetes Complications. 2009 Sep-Oct;23(5):310-6. doi: 10.1016/j.jdiacomp.2008.02.009. Epub 2008 Apr 3.

Cardioprotective effect of vitamin E: rescues of diabetes-induced cardiac malfunction, oxidative stress, and apoptosis in rat.

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Department of Physiology, Faculty of Medicine, Urmia University of Medical Science, Urmia, Iran.



This study was designed to assess the effect of vitamin E on cardiac autonomic neuropathy, cardiomyocyte apoptosis, and the status of oxidative stress in the heart under hyperglycemic conditions, in vivo.


Wistar male rats (n=16) were made hyperglycemic by streptozotocin at 6 months of age. Normal Wistar rats (n=8) of the same age were used as the control group. Diabetic rats were divided into two groups, nontreated and those treated with vitamin E (300 mg/day). Stable hyperglycemic status was proved by levels of blood sugar and HbA(1c). Lipid peroxidation, protein oxidation, and cellular antioxidant defense were measured by 8-isoprotane, protein carbonyl content, and superoxide dismutase (SOD) activity, respectively.


Cardiac complications such as autonomic neuropathy as prolonged QT interval along with significant increases in level of 8-isoprotane, protein carbonyl content, and SOD activity were observed after 6 weeks. Structural abnormality was also observed as severe induction of apoptosis in cardiomyocytes.


Significant decline in apoptosis, lipid peroxidation, protein oxidation, and QT interval resulted from vitamin E administration, which strongly implies that this radical scavenger may promote a convalescing effect on diabetic cardiomyopathy through the attenuation of oxidative stress and abrogation of apoptotic signals, which was verified by restoring normal QT interval.

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