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D.L. Gierhart, R. Kowluru; Administration of Zeaxanthin Inhibits Diabetes–Induced Metabolic Abnormalities in the Retina . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1746.
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Oxidative damage is involved in the pathogenesis of retinopathy in diabetes. Recent studies have shown that dietary carotenoids are specifically concentrated within ocular tissues, and may play important roles in maintaining the integrity of these structures. Serum levels of lutein/zeaxanthin (Zx) and lycopene are significantly lower in the diabetics. The purpose of this study is to evaluate the potential protective effects of Zx against retinal oxidative stress in diabetes.
A group of Lewis rats (200–225 BW, male), made diabetic by streptozotocin injection, were divided into three groups: group one received normal powdered Purina diet, and groups two and three received powdered diet supplemented with 0.02% or 0.1% Zx respectively. Age–matched normal rats served as controls. At two months of diabetes the levels of oxidatively modified DNA (8–hydroxy guanosine, 8OHdG),lipoperoxides(LPO), glutathione (GSH) , nitrotyrosine, and the activity of superoxide dismutase (SOD) were measured in the retina.
Zx supplementation for two months to diabetic rats inhibited increase in retinal oxidative stress and nitrative stress. The levels of 8–OHdG ,LPO, nitrotyrosine, and the activity of SOD in Zx–treated diabetic rat retina were similar to those obtained from the normal control rat retina, and these values were significantly different from those obtained from diabetic rats without any supplementation. However, Zx administration did not significantly inhibit diabetes–induced decrease in retinal GSH levels. Both, 0.02% and 0.1% Zx had similar effects on the parameters of oxidative stress and nitrative stress, and these effects were achieved without ameliorating the severity of hyperglycemia.
Zx significantly inhibits diabetes–induced retinal oxidative damage, and nitration of proteins. Thus, Zx supplementation could represent a supplemental therapy to inhibit the development of retinopathy in diabetes.
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