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


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Shirpoor
Alireza
A
Department of Physiology, Faculty of Medicine, Urmia University of Medical Science, Urmia, Iran.
Salami
Siamak
S
Khadem-Ansari
Mohammad H
MH
Ilkhanizadeh
Behrouz
B
Pakdel
Firouz Ghaderi
FG
Khademvatani
Kamal
K
D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D009202:Cardiomyopathies / Q000209:etiology / Q000503:physiopathology*; D002316:Cardiotonic Agents / Q000008:administration & dosage*; D002374:Catalase / Q000378:metabolism; D016009:Chi-Square Distribution; D048909:Diabetes Complications / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental; D003929:Diabetic Neuropathies / Q000503:physiopathology*; D004562:Electrocardiography; D006321:Heart / Q000503:physiopathology*; D006943:Hyperglycemia / Q000503:physiopathology; D020287:In Situ Nick-End Labeling; D028421:Isoprostanes / Q000032:analysis; D015227:Lipid Peroxidation; D008297:Male; D009206:Myocardium / Q000737:chemistry / Q000201:enzymology / Q000473:pathology; D009929:Organ Size; D018384:Oxidative Stress / Q000502:physiology*; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D014810:Vitamin E / Q000008:administration & dosage* / Q000502:physiology; D015430:Weight Gain
D002316:Cardiotonic Agents; D028421:Isoprostanes; D014810:Vitamin E; D002374:Catalase; D013482:Superoxide Dismutase