Research Article Oxidative Stress and Histological Changes in a Model of Retinal Phototoxicity in Rabbits Manuel Saenz-de-Viteri, 1,2 Henar Heras-Mulero, 1,2 Patricia Fernández-Robredo, 1 Sergio Recalde, 1 María Hernández, 1 Nicholas Reiter, 1 Maite Moreno-Orduña, 1 and Alfredo García-Layana 1,2 1 Experimental Ophthalmology Laboratory, School of Medicine, University of Navarra, 1 Irunlarrea Street, 31008 Pamplona, Spain 2 Department of Ophthalmology, Cl´ ınica Universidad de Navarra, School of Medicine, University of Navarra, 36 Pio XII Avenue, 31008 Pamplona, Spain Correspondence should be addressed to Alfredo Garc´ ıa-Layana; aglayana@unav.es Received 14 February 2014; Revised 14 April 2014; Accepted 22 April 2014; Published 27 May 2014 Academic Editor: Kota V. Ramana Copyright © 2014 Manuel Saenz-de-Viteri et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Photochemical damage occurs afer an exposure to high energy radiation within the visible spectrum of light, causing morphological changes in the retina and the formation of superoxide anion. In this study we created a model of phototoxicity in rabbits. Animals were exposed to a light source for 120 minutes and were sacrifced immediately or one week afer exposure. Outer nuclear layer and neurosensory retina thickness measurements and photoreceptor counting were performed. Caspase-1 and caspase-3 were assessed by immunohistochemistry. Dihydroethidium was used to evaluate in situ generation of superoxide and thiobarbituric acid reactive substances were measured in retinal homogenates as indicators of lipid peroxidation. Te total antioxidant capacity and oxidative ratio were also determined. Retinas from rabbits exposed to light showed higher levels of lipid peroxidation than the unexposed animals and a decrease in outer nuclear layer and neurosensory retina thickness. Our study demonstrates that light damage produces an increase in retinal oxidative stress immediately afer light exposure that decreases one week afer exposure. However, some morphological alterations appear days afer light exposure including apoptotic phenomena. Tis model may be useful in the future to study the protective efect of antioxidant substances or new intraocular lenses with yellow flters. 1. Introduction Photochemical damage occurs afer an exposure to high energy radiation with a wavelength within the visible spec- trum of light. It has been demonstrated that the blue portion of the visible spectrum of light is the most harmful, producing disturbances of the outer blood retinal barrier in the retinal pigmented epithelium (RPE) [1]. At the retinal level, exposure to light causes an increase in phagocytosis of photoreceptor outer segments (POS) [2] and induces the formation of superoxide anion by the RPE [3]. Tissues with a high proportion of membrane lipids and a high tissue oxygen concentration are most sensitive to damage by oxidative stress [4]. Te retina has a high oxygen tension (70 mmHg) which makes it very vulnerable to oxidative stress [5]. Moreover, the retina and more specifcally the POS possess very high levels of polyunsaturated fatty acids which further increases the sensitivity to oxidative damage and lipid peroxidation of cell membranes [6, 7] as well as phenomena of cell death (apoptosis or necrosis) [8]. Evidence suggests that excessive light exposure plays an important role in the development and progression of age related macular degeneration (AMD) [913]. Lipofuscin, a target molecule for phototoxic damage, accumulates in the retina with age, making elderly people more susceptible to light damage [9]. On the contrary, the human lens accumulates yellow chromophores with aging that reduce the transmission of blue and UV light to the retina [9, 10]. However, removal of the lens by cataract surgery, a common Hindawi Publishing Corporation Oxidative Medicine and Cellular Longevity Volume 2014, Article ID 637137, 10 pages http://dx.doi.org/10.1155/2014/637137