Palm vitamin E reduces oxidative stress, and physical and morphological alterations of erythrocyte membranes in streptozotocin-induced diabetic rats

We investigated the effects of diabetes mellitus and antioxidant treatment on the sensory and reflex function of cardiac chemosensory nerves in rats. Diabetes was induced by streptozotocin (STZ; 85 mg/kg ip). Subgroups of sham- and STZ-treated rats were chronically treated with an antioxidant, vitamin E (60 mg/kg per os daily, started 2 days before STZ). Animals were studied 6–8 wk after STZ injection. We measured renal sympathetic nerve activity (RSNA), mean arterial blood pressure (MABP), and cardiac vagal and sympathetic afferent activities in response to stimulation of chemosensitive sensory nerves in the heart by epicardial application of capsaicin (Caps) and bradykinin (BK). In cardiac sympathetic-denervated rats, Caps and BK (1–10.0 μg) evoked a vagal afferent mediated reflex depression of RSNA and MABP, which was significantly blunted in STZ-treated rats ( P < 0.05). In vagal-denervated rats, Caps and BK (1–10.0 μg) evoked a sympathetic afferent-mediated reflex elevation of RSNA and MABP, which also was significantly blunted in STZ-treated rats ( P< 0.05). Chronic vitamin E treatment effectively prevented these cardiac chemoreflex defects in STZ-treated rats without altering resting blood glucose or hemodynamics. STZ-treated rats with insulin replacement did not exhibit impaired cardiac chemoreflexes. In afferent studies, Caps and BK (0.1 g-10.0 μg) increased cardiac vagal and sympathetic afferent nerve activity in a dose-dependent manner in sham-treated rats. These responses were significantly blunted in STZ-treated rats. Vitamin E prevented the impairment of afferent discharge to chemical stimulation in STZ rats. The following were concluded: STZ-induced, insulin-dependent diabetes in rats extensively impairs the sensory and reflex properties of cardiac chemosensitive nerve endings, and these disturbances can be prevented by chronic treatment with vitamin E. These results suggest that oxidative stress plays an important role in the neuropathy of this autonomic reflex in diabetes.

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Effects of Vitamin E Supplementation on Oxidative Stress in Streptozotocin Induced Diabetic Rats: Investigation of Liver and Plasma

Yonsei Medical Journal ◽

10.3349/ymj.2004.45.4.703 ◽

2004 ◽

Vol 45 (4) ◽

pp. 703 ◽

Cited By ~ 48

Author(s):

Arzu Seven ◽

Sava Güzel ◽

Oktay Seymen ◽

Sabiha Civelek ◽

Murat Bolayırlı ◽

...

Keyword(s):

Oxidative Stress ◽

Vitamin E ◽

Diabetic Rats ◽

Vitamin E Supplementation

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Effects of Estrogen Replacement Therapy with Vitamin E on Oxidative Stress in Hepatic and Pancreatic Tissues of Ovariectomized Diabetic Rats

Journal of Animal and Veterinary Advances ◽

10.3923/javaa.2010.2955.2962 ◽

2010 ◽

Vol 9 (23) ◽

pp. 2955-2962 ◽

Cited By ~ 3

Author(s):

Mehmet Cay ◽

Mustafa Ulas

Keyword(s):

Oxidative Stress ◽

Vitamin E ◽

Replacement Therapy ◽

Estrogen Replacement Therapy ◽

Diabetic Rats ◽

Estrogen Replacement

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Vitamin E supplementation protects erythrocyte membranes from oxidative stress in healthy Chinese middle-aged and elderly people

Nutrition Research ◽

10.1016/j.nutres.2012.03.012 ◽

2012 ◽

Vol 32 (5) ◽

pp. 328-334 ◽

Cited By ~ 26

Author(s):

Yongye Sun ◽

Aiguo Ma ◽

Yong Li ◽

Xiuxia Han ◽

Qiuzhen Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Vitamin E ◽

Elderly People ◽

Erythrocyte Membranes ◽

Middle Aged ◽

Healthy Chinese ◽

Vitamin E Supplementation

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Oxidative Stress As A Common Mediator for Apoptosis Induced-Cardiac Damage in Diabetic Rats

The Open Cardiovascular Medicine Journal ◽

10.2174/1874192400802010070 ◽

2008 ◽

Vol 2 (1) ◽

pp. 70-78 ◽

Cited By ~ 22

Author(s):

Mohammad M Dallak ◽

Dimitri P Mikhailidis ◽

Mohamed A Haidara ◽

Ismaeel M Bin-Jaliah ◽

Olaa M Tork ◽

...

Keyword(s):

Oxidative Stress ◽

Electron Microscopy ◽

Vitamin E ◽

Cardiac Function ◽

Diabetic Rats ◽

Cardiac Complications ◽

Cardiac Damage ◽

Group I ◽

Markers Of Oxidative Stress

Abstract:Aim:To investigate the possible role of oxidative stress as a common mediator of apoptosis and cardiac damage in diabetes.Materials and Methods:This experimental work was conducted on 5 groups of Wistar rats. Group I was the control group. Diabetes type 1 was induced in other groups (by streptozotocin) and animals received insulin or vitamin E (300 mg /kg body weight), both insulin and vitamin E, or no treatment for 4 weeks according to their group. At the end of the study, serum and cardiac tissues were examined for biochemical parameters of cardiac function, oxidative stress and apoptosis. Electron microscopy pictures of cardiac tissue were also evaluated for signs of cardiac damageResults:Markers of oxidative stress, apoptosis, inflammation as well as manifestations of cardiac damage as assessed by electron microscopy were significantly decreased in rats treated with both insulin and vitamin E when compared with untreated diabetic rats or rats treated with either insulin or vitamin E aloneConclusion:Administration of both vitamin E and insulin was effective in reducing markers of oxidative stress and apoptosis and improving parameters of cardiac function in experiments animals. Antioxidants might prove beneficial as an adjuvant treatment in addition to insulin in type 1 diabetes associated with manifestations of cardiac complications

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Enhanced mitochondrial testicular antioxidant capacity in Goto-Kakizaki diabetic rats: role of coenzyme Q

AJP Cell Physiology ◽

10.1152/ajpcell.2001.281.3.c1023 ◽

2001 ◽

Vol 281 (3) ◽

pp. C1023-C1028 ◽

Cited By ~ 33

Author(s):

Carlos M. Palmeira ◽

Dario L. Santos ◽

Raquel Seiça ◽

António J. Moreno ◽

Maria S. Santos

Keyword(s):

Oxidative Stress ◽

Diabetes Mellitus ◽

Vitamin E ◽

Antioxidant Capacity ◽

Coenzyme Q ◽

Reactive Oxygen Species Generation ◽

Diabetic Rats ◽

Insulin Dependent ◽

Mitochondrial Glutathione ◽

Insulin Dependent Diabetic

Because diabetes mellitus is associated with impairment of testicular function, ultimately leading to reduced fertility, this study was conducted to evaluate the existence of a cause-effect relationship between increased oxidative stress in diabetes and reduced mitochondrial antioxidant capacity. The susceptibility to oxidative stress and antioxidant capacity (in terms of glutathione, coenzyme Q, and vitamin E content) of testis mitochondrial preparations isolated from Goto-Kakizaki (GK) non-insulin-dependent diabetic rats and from Wistar control rats, 1 yr of age, was evaluated. It was found that GK mitochondrial preparations showed a lower susceptibility to lipid peroxidation induced by ADP/Fe2+, as evaluated by oxygen consumption and reactive oxygen species generation. The decreased susceptibility to oxidative stress in diabetic rats was associated with an increase in mitochondrial glutathione and coenzyme Q9 contents, whereas vitamin E was not changed. These results demonstrate a higher antioxidant capacity in diabetic GK rats. We suggest this is an adaptive response of testis mitochondria to the increased oxidative damage in diabetes mellitus.

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