Letter to the Editor Topography of retinal damage in light-exposed albino rats Masaki Tanito a, b, c, * , Sachiko Kaidzu c , Akihiro Ohira c , Robert E. Anderson a, b, d, ** a Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA b Dean A. McGee Eye Institute, Oklahoma City, Oklahoma, USA c Department of Ophthalmology, Shimane University Faculty of Medicine, Izumo, Shimane, Japan d Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA article info Article history: Received 25 March 2008 Accepted in revised form 4 June 2008 Available online 11 June 2008 Keywords: retinal light damage outer nuclear layer (ONL) thickness retinal topography abstract Previous studies have shown that retinal damage induced by damaging light exposure is more severe in superior retina than inferior retina when measured along the vertical meridian of eyes. However, the extent of retinal damage over all retinal regions is not clear. Albino rats were exposed to bright light (5000 lux for 6 h) and eyes removed 7 days later. Outer nuclear layer (ONL) thickness was measured along four different meridians; temporal-to-nasal (T–N), superior-to-inferior (S–I), superiotemporal-to- inferionasal (ST–IN), and superionasal-to-inferiotemporal (SN–IT). As reported previously, superior retina is more severely damaged than inferior retina along the S–I meridian. In addition, we found that the temporal retina is more severely damaged than nasal retina on the T–N meridian. Color-coded topo- graphic maps clearly revealed that thinning of ONL was greatest at 1–1.5 mm superior and superi- otemporal to the optic nerve head and that most damage was in the superiotemporal region of the fundus. For consistency in quantification of ONL thickness, using retinal sections cut along the S–I me- ridian is preferable to using those along the T–N meridian, since minor orientations to superior or inferior directions along the T–N meridian may cause greater variations in measured ONL thickness values in this experimental model. Ó 2008 Elsevier Ltd. All rights reserved. Previous experimental studies using bright light exposure to rodent eyes have shown that light stress causes photoreceptor cell damage (Noell et al., 1966; Noell and Albrecht, 1971) and that the apoptotic pathway, the common fate of photoreceptors in retinitis pigmentosa and age-related macular degeneration, is the main course of light-induced cell death (Wenzel et al., 2005). Intense light exposure causes lipid peroxidation of retinal tissues (Wiegand et al., 1983; Organisciak et al., 1992; Tanito et al., 2006) and oxi- dative stress is likely to be involved in the pathogenesis of light- induced retinal damage (Organisciak et al., 1999; Ranchon et al., 2003; Tanito et al., 2007b). Thus, light-induced damage in the albino rat is a suitable model system to study retinal degeneration and other retinal pathologies related to oxidative stress (Ranchon et al., 2003). It is well established that the severity of retinal damage induced by light has great variation among retinal regions. Along the ver- tical meridian of the eye, the superior retina is more severely damaged than the inferior, and the central retina is more severely damaged than peripheral (LaVail et al., 1987; Rapp and Smith, 1992; Reme et al., 1994; Organisciak et al., 1999; Ranchon et al., 2003). In the current study, topographic analysis of outer nuclear layer (ONL) thickness in retinas from damaging light-exposed and light- unexposed rats was performed to examine the regional distribution of retinal damage over entire retina. All procedures were carried out according to the ARVO State- ment for the Use of Animals in Ophthalmic and Vision Research and the University of Oklahoma Health Sciences Center (OUHSC) Guidelines for Animals in Research. All protocols were reviewed and approved by the Institutional Animal Care and Use Committees of the OUHSC and the Dean A. McGee Eye Institute. Sprague– Dawley (Harlan Sera-Lab, Indianapolis, Indiana) rats were born and raised in our vivarium, and kept under dim cyclic light (5 lux, 12 h on/off, 7AM–7PM) prior to experimentation. Unanesthetized rats (5–6 weeks of age) were exposed to 5000 lux diffuse, cool, white fluorescent light for 6 h as described previously (Tanito et al., 2007a). After exposure, the rats were returned to the dim cyclic light environment for 7 days, after which they were euthanized and * Corresponding author. Department of Ophthalmology, Shimane University Faculty of Medicine, Enya 89-1, Izumo, Shimane, 693-8501, Japan. Tel.: þ81 853 20 2284; fax: þ81 853 20 2278. ** Corresponding author. Department of Ophthalmology, University of Oklahoma Health Sciences Center, 608 S. L. Young Boulevard,Oklahoma City, Oklahoma 73104, USA. Tel.: þ1 405 271 8250; fax: þ1 405 271 8128. E-mail addresses: tanito-oph@umin.ac.jp, mtanito@med.shimane-u.ac.jp (M. Tanito), robert-anderson@ouhsc.edu (R.E. Anderson). Contents lists available at ScienceDirect Experimental Eye Research journal homepage: www.elsevier.com/locate/yexer 0014-4835/$ – see front matter Ó 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.exer.2008.06.002 Experimental Eye Research 87 (2008) 292–295