Changes in Isoprenaline-Induced Endothelium-Dependent and -Independent Relaxations of Aorta in Long-Term STZ-Diabetic Rats: Reversal Effect of Dietary Vitamin E

Karasu, Çi̇men; Ozansoy, Gülgun; Bozkurt, Onur; Erdoğan, Deniz; Ömeroğlu, Suna

doi:10.1016/s0306-3623(96)00577-0

Cited by 21 publications

(11 citation statements)

References 26 publications

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“…This event would predispose the vessel to develop atherosclerotic lesions due to the potential consequence of increased macromolecular permeability and intimal proliferation via the development of vasospasm, thrombosis and recruitment of platelets and leukocytes [91, 94]. In this respect, we confirmed the monocyte adhesion to the endothelial cells and impaired morphology of diabetic aorta by electron microscopy [63, 64, 68, 95]. Beside monocytes, there are many other inhibitors of the biological activity of NO, such as decreased L-arginine uptake, decreased co-factors (Ca 2+ , calmodulin, BH4), inhibition of electron flow (nicotinamide adenine dinucleotide phosphate; NADPH, flavins), inhibition of NOS expression, inhibition of substrate binding to NOS, and NO scavengers [97, 98].…”

Section: Impaired Vascular Reactivity In Dm: Role Of Endothelial Cellssupporting

confidence: 58%

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Glycoxidative Stress and Cardiovascular Complications in Experimentally-Induced Diabetes: Effects of Antioxidant Treatment

Karasu¹

2010

TOCMJ

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Diabetes mellitus (DM) is a common metabolic disease, representing a serious risk factor for the development of cardiovascular complications, such as coronary heart disease, peripheral arterial disease and hypertension. Oxidative stress (OS), a feature of DM, is defined as an increase in the steady-state levels of reactive oxygen species (ROS) and may occur as a result of increased free radical generation and/or decreased anti-oxidant defense mechanisms. Increasing evidence indicates that hyperglycemia is the initiating cause of the tissue damage in DM, either through repeated acute changes in cellular glucose metabolism, or through long-term accumulation of glycated biomolecules and advanced glycation end products (AGEs). AGEs are formed by the Maillard process, a non-enzymatic reaction between ketone group of the glucose molecule or aldehydes and the amino groups of proteins that contributes to the aging of proteins and to the pathological complications of DM. In the presence of uncontrolled hyperglycemia, the increased formation of AGEs and lipid peroxidation products exacerbate intracellular OS and results in a loss of molecular integrity, disruption in cellular signaling and homeostasis, followed by inflammation and tissue injury such as endothelium dysfunction, arterial stiffening and microvascular complications. In addition to increased AGE production, there is also evidence of multiple pathways elevating ROS generation in DM, including; enhanced glucose auto-oxidation, increased mitochondrial superoxide production, protein kinase C-dependent activation of NADPH oxidase, uncoupled endothelial nitric oxide synthase (eNOS) activity, increased substrate flux through the polyol pathway and stimulation of eicosanoid metabolism. It is, therefore, not surprising that the correction of these variables can result in amelioration of diabetic cardiovascular abnormalities. A linking element between these phenomena is cellular redox imbalance due to glycoxidative stress (GOS). Thus, recent interest has focused on strategies to prevent, reverse or retard GOS in order to modify the natural history of diabetic cardiovascular abnormalities. This review will discuss the links between GOS and diabetes-induced cardiovascular disorders and the effect of antioxidant therapy on altering the development of cardiovascular complications in diabetic animal models.

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Section: Impaired Vascular Reactivity In Dm: Role Of Endothelial Cellssupporting

confidence: 58%

“…These recoveries were associated with the amelioration in vascular and cardiac metabolism/function [22, 46, 63, 64, 69, 95, 119, 142, 147, 148, 154, 159-161]. We have previously focused on investigating the effects of dietary supplementation of the antioxidants vitamin E, alpha-lipoic acid and vitamin A.…”

Section: Glycoxidative Stress: a Key Therapeutic Target?mentioning

confidence: 99%

Glycoxidative Stress and Cardiovascular Complications in Experimentally-Induced Diabetes: Effects of Antioxidant Treatment

Karasu¹

2010

TOCMJ

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“…During diabetes, persistent hyperglycemia causes an excessive endogenous formation of free radicals apparently overcomes cellular antioxidant defense mechanisms, resulting in free radicals-initiated modification of lipids, proteins, carbohydrates and DNA (28). One of the commonly findings of the oxidative stress is the increased production of malondialdehyde as TBARS levels which has been found in the plasma and various tissues of diabetic patients and animals (29,30,31,32). In agreement with previous studies, we also found that TBARS levels of plasma were increased in diabetic group compared with control group.…”

Section: Discussionsupporting

confidence: 92%

The Effects of Vitamin E Treatment on Tracheal Reactivity and Some Biochemical Parameters in Diabetic Rats : Di̇yabeti̇k Siçanlarda, Vi̇tami̇n E Tedavi̇si̇ni̇n Trakeal Reakti̇vi̇te Ve Bazi Bi̇yoki̇msal Paramet

Ozansoy¹

2003

Ankara Universitesi Eczacilik Fakultesi Dergisi

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“…In another diabetes rat model, vitamin E attenuated, but did not completely prevent, diabetes-induced endothelial dysfunction [48]. Two-month, dietary, vitamin E supplementation in the diabetic rat reduced lipid peroxide levels [49]. It remains unclear, however, whether such positive effects of vitamin E might be attenuated in models with longer duration of the disease.…”

Section: Vitamin E and Diabetesmentioning

confidence: 99%

Vitamin E, diabetes and related diseases: an update

Vignini

Alidori

Montesi

et al. 2010

Mediterr J Nutr Metab

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Natural vitamin E is a mixture of tocopherols and tocotrienols synthesized only by plants. It is very difficult to determine the optimal dietary intake of vitamin E, but there is a general agreement indicating a level of 8 mg/ day (12-15 IU). This value seems to be sufficient only to prevent deficiency syndromes of vitamin E. In humans, vitamin E is absorbed together with nutritional lipids in the proximal part of the intestine and released in the lymph within chylomicrons. Vitamin E supplementation, as other minerals and vitamins, is able to participate in the decrease of oxidative stress in diabetic patients by improving glycemic control and/or by other mechanisms related to its antioxidant activity, therefore cooperating to the control of diabetic complications. Many interventional trials evaluating the effect of antioxidant supplementation on insulin resistance, plasma glucose levels and risk of T2D give inconsistent results. At present, a controversial hypothesis about the role played by vitamin E supplementation still exists. In fact, while laboratory data report great cellular and biochemical beneficial actions, clinical trials have failed to support these claims. Concerning clinical trials, the discrepancies have been attributed to differences in selection of individuals, dosage, chemical forms of vitamin E, duration of treatment, stage of the disease and geographical area. Because of these variables, further studies aimed to clarify the relationship between diabetes, cardiovascular risk factors and vitamin E are necessary.

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Changes in Isoprenaline-Induced Endothelium-Dependent and -Independent Relaxations of Aorta in Long-Term STZ-Diabetic Rats: Reversal Effect of Dietary Vitamin E

Cited by 21 publications

References 26 publications

Glycoxidative Stress and Cardiovascular Complications in Experimentally-Induced Diabetes: Effects of Antioxidant Treatment

Glycoxidative Stress and Cardiovascular Complications in Experimentally-Induced Diabetes: Effects of Antioxidant Treatment

The Effects of Vitamin E Treatment on Tracheal Reactivity and Some Biochemical Parameters in Diabetic Rats : Di̇yabeti̇k Siçanlarda, Vi̇tami̇n E Tedavi̇si̇ni̇n Trakeal Reakti̇vi̇te Ve Bazi Bi̇yoki̇msal Paramet

Vitamin E, diabetes and related diseases: an update

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