Light-Induced Retinal Degeneration Is Prevented by Zinc, a Component in the Age-related Eye Disease Study Formulation

• Type of Material: Article
• Authors: Daniel Organisciak, Wright State University; Paul Wong, Emory University; Christine Rapp, Wright State University; Ruth Darrow, Wright State University; Alison Ziesel, Emory University; Rekha Rangarajan, Alcon Research Ltd; John Lang, Alcon Research Ltd
• Language: English
• Date: 2012-11-01
• Publisher: Wiley: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2012 Wiley Periodicals, Inc. Photochemistry and Photobiology
• Final Published Version (URL): http://dx.doi.org/10.1111/j.1751-1097.2012.01134.x
• Title of Journal or Parent Work: Photochemistry and Photobiology
• ISSN: 0031-8655
• Volume: 88
• Issue: 6
• Start Page: 1396
• End Page: 1407
• Grant/Funding Information: This study was funded by support from Alcon Research Ltd. and the Ohio Lions Research Foundation (DTO), a NEI Core Grant for Vision Research (P30 EY 006360) and an unrestricted departmental grant from Research to Prevent Blindness (RPB) Department of Ophthalmology, Emory School of Medicine, Atlanta, GA, USA (PW).
• Keywords: MACULAR DEGENERATION; INDUCTION; Biophysics; INDUCED PHOTORECEPTOR; DEFICIENCY; FACTOR-H; DAMAGE; OXIDATIVE STRESS; RATS; EPITHELIAL-CELLS; PIGMENT EPITHELIUM; Life Sciences & Biomedicine; Biochemistry & Molecular Biology; Science & Technology
• Research Categories: Biology, Molecular; Chemistry, Biochemistry

Abstract

Mineral supplements are often included in multivitamin preparations because of their beneficial effects on metabolism. In this study, we used an animal model of light-induced retinal degeneration to test for photoreceptor cell protection by the essential trace element zinc. Rats were treated with various doses of zinc oxide and then exposed to intense visible light for as long as 8 h. Zinc treatment effectively prevented retinal light damage as determined by rhodopsin and retinal DNA recovery, histology and electrophoretic analysis of DNA damage and oxidized retinal proteins. Zinc oxide was particularly effective when given before light exposure and at doses two- to four-fold higher than recommended by the age-related eye disease study group. Treated rats exhibited higher serum and retinal pigment epithelial zinc levels and an altered retinal gene expression profile. Using an Ingenuity database, 512 genes with known functional annotations were found to be responsive to zinc supplementation, with 45% of these falling into a network related to cellular growth, proliferation, cell cycle and death. Although these data suggest an integrated and extensive regulatory response, zinc induced changes in gene expression also appear to enhance antioxidative capacity in retina and reduce oxidative damage arising from intense light exposure.