Retina Light Damage in Abca 4 and Rpe 65 rd 12 Mice

Citation: Wu L, Ueda K, Nagasaki T, Sparrow JR. Light damage in Abca4 and Rpe65 mice. Invest Ophthalmol Vis Sci. 2014;55:1910–1918. DOI:10.1167/iovs.14-13867 PURPOSE. Bisretinoids form in photoreceptor cells and accumulate in retinal pigment epithelium (RPE) as lipofuscin. To examine the role of these fluorophores as mediators of retinal light damage, we studied the propensity for light damage in mutant mice having elevated lipofuscin due to deficiency in the ATP-binding cassette (ABC) transporter Abca4 (Abca4 / mice) and in mice devoid of lipofuscin owing to absence of Rpe65 (Rpe65). METHODS. Abca4 / , Rpe65, and wild-type mice were exposed to 430-nm light to produce a localized lesion in the superior hemisphere of retina. Bisretinoids of RPE lipofuscin were measured by HPLC. In histologic sections, outer nuclear layer (ONL) thickness was measured as an indicator of photoreceptor cell degeneration, and RPE nuclei were counted.