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Christian Sheline, Shi Bai; Light-induced Retinal Damage: Role Of Dietary Zinc And Zinc Binding Proteins. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2562.
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Intense visible light induces severe damage (LD) to retina and serves as a model of human oxidation-induced, light-potentiated retinal degenerative diseases such as AMD. Our previous study on LD suggests the involvement of zinc toxicity in the death of photoreceptor and RPE cells after intense light. However, the AREDS trial shows that chronic dietary Zn2+ supplementation (ZnE) delays the progression of AMD. Zn2+ is present physiologically in layers of the retina: in particular in the rod segments bound to rhodopsin, the outer plexiform layer, and RPE cells. The loosely bound, histochemically reactive Zn2+ plays important roles in the visual cycle, dark/light adaptation, neuro-transmission, and intracellular metabolism. So we examined the effects of manipulating zinc levels on retinal zinc binding protein levels (ZBP), and light-induced Zn2+ accumulation and damage in rodents, by both reducing and increasing dietary zinc.
Sprague Dawley or CD1 albino rats or mice were fed for 3 wk with a 1 ppm zinc diet (ZnR), a 60 ppm zinc diet (ZnN, normal), or a 200 ppm zinc diet (ZnE) and rats were exposed to 18 kLux of white light for 4 h. Retinal extracts from mice were purified by Zn2+ affinity, and analyzed by 2D gels. ZBP’s were identified by LC-MS.
Both a ZnR and a ZnE diet attenuated Zn2+ accumulation and photoreceptor degeneration after LD compared to ZnN. ZnE increases levels of a group of low MW ZBP’s. Three groups of retinal ZBP proteins were identified by proteomics and westerns: visual cycle proteins, energy metabolic enzymes, and chaperone proteins.
Zn2+ homeostasis and ZBP’s are important in the visual cycle, stress, LD, and retinal health and disease. Dietary Zn2+ manipulations which chronically increase ZBP’s, or acutely reduce the retinal Zn2+ accumulation will attenuate retinal injury in rodents, and may explain the efficacy of zinc supplementation on AMD in humans.
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