Effects of Stobadine and Vitamin E in Diabetes-Induced Retinal Abnormalities: Involvement of Oxidative Stress

Yülek, Fatma; Or, Meral; Özoğul, Candan; Isik, Asli Ceylan; Arı, Nuray; Štefek, Milan; Bauer, V.; Karasu, Çi̇men

doi:10.1016/j.arcmed.2007.02.006

Cited by 40 publications

(41 citation statements)

References 45 publications

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“…Supplementation with vitamin E reduces basement membrane thickening in diabetic rat retina and reduces VEGF and aldose reductase activity, the abnormalities associated with diabetic retinopathy [127]. We have shown that these vitamins prevent inhibition of retinal glutathione reductase, glutathione peroxidase, and SOD activities and the development of retinopathy in diabetic rats [35,38].…”

Section: Antioxidantsmentioning

confidence: 76%

Oxidative stress and diabetic retinopathy: Pathophysiological mechanisms and treatment perspectives

Madsen–Bouterse

Kowluru

2008

Rev Endocr Metab Disord

263

184

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Retinopathy is one of the most severe ocular complications of diabetes and is a leading cause of acquired blindness in young adults. The cellular components of the retina are highly coordinated but very susceptible to the hyperglycemic environment. The microvasculature of the retina responds to hyperglycemic milieu through a number of biochemical changes, including increased oxidative stress and polyol pathway, PKC activation and advanced glycation end product formation. Oxidative stress is considered as one of the crucial contributors in the pathogenesis of diabetic retinopathy, but oxidative stress appears to be highly interrelated with other biochemical imbalances that lead to structural and functional changes and accelerated loss of capillary cells in the retinal microvasculature and, ultimately, pathological evidence of the disease. One such potential connection that links oxidative stress to metabolic alterations is gyceraldehyde-3-phosphate dehydrogenase whose activity is impaired in diabetes, and that results in activation of other major pathways implicated in the pathogenesis of diabetic retinopathy. Alterations associated with oxidative stress offer many potential therapeutic targets making this an area of great interest to the development of safe and effective treatments for diabetic retinopathy. Animal models of diabetic retinopathy have shown beneficial effects of antioxidants on the development of retinopathy, but clinical trials (though very limited in numbers) have provided somewhat ambiguous results. Although antioxidants are being used for other chronic diseases, controlled clinical trials are warranted to investigate potential beneficial effects of antioxidants in the development of retinopathy in diabetic patients.

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Section: Antioxidantsmentioning

confidence: 76%

Oxidative stress and diabetic retinopathy: Pathophysiological mechanisms and treatment perspectives

Madsen–Bouterse

Kowluru

2008

Rev Endocr Metab Disord

263

184

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“…In an animal model of retinal I/R injury, reduced levels of oxidative stress marker such as MDA together with an inactivation of caspase-3 but increased levels of GSH were noted with vitamin E treatment [77–81]. In experimental DR models, oral intake of antioxidants, including vitamin E, significantly reduced lipid peroxidation and arrested retinal abnormalities in streptozotocin (STZ)-induced diabetic rats [82]. Intake of micronutrients based on the AREDS formula (vitamin E, ascorbic acid, beta-carotene, zinc, and copper) inhibited the increases in nitrotyrosine and inducible NOS and decreases in MnSOD in STZ-induced diabetic rats [83].…”

Section: Antioxidants In Ischemic Retinopathiesmentioning

confidence: 99%

Hypoxia-Induced Oxidative Stress in Ischemic Retinopathy

2012

Oxidative Medicine and Cellular Longevity

111

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Oxidative stress plays a crucial role in the pathogenesis of retinal ischemia/hypoxia, a complication of ocular diseases such as diabetic retinopathy (DR) and retinopathy of prematurity (ROP). Oxidative stress refers to the imbalance between the production of reactive oxygen species (ROS) and the ability to scavenge these ROS by endogenous antioxidative systems. Free radicals and ROS are implicated in the irreversible damage to cell membrane, DNA, and other cellular structures by oxidizing lipids, proteins, and nucleic acids. Anti-oxidants that can inhibit the oxidative processes can protect retinal cells from ischemic/hypoxic insults. In particular, treatment using anti-oxidants such as vitamin E and lutein, inhibition of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) or related signaling pathways, and administration of catalase and superoxide dismutase (SOD) are possible therapeutic regimens for DR, ROP, and other retinal ischemic diseases. The role of oxidative stress in the pathogenesis of DR and ROP as well as the underlying mechanisms involved in the hypoxia/ischemia-induced oxidative damage is discussed. The information provided will be beneficial in understanding the underlying mechanisms involved in the pathogenesis of the diseases as well as in developing effective therapeutic interventions to treat oxidative stress-induced damages.

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“…Experiments from “the ADIC Study Group”, observed the effectiveness of exogenous antioxidant treatments in the recovery of OS markers and endogenous antioxidant enzyme activities in STZ-diabetic rats [22, 63, 64, 154, 159-161]. 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].…”

Section: Glycoxidative Stress: a Key Therapeutic Target?mentioning

confidence: 99%

“…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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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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Effects of Stobadine and Vitamin E in Diabetes-Induced Retinal Abnormalities: Involvement of Oxidative Stress

Cited by 40 publications

References 45 publications

Oxidative stress and diabetic retinopathy: Pathophysiological mechanisms and treatment perspectives

Oxidative stress and diabetic retinopathy: Pathophysiological mechanisms and treatment perspectives

Hypoxia-Induced Oxidative Stress in Ischemic Retinopathy

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

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