Figure 5. Light damage in Rdh13^-/- mice. Light damage was induced in Rdh13^+/+ and Rdh13^−/− mice by 48 h exposure to diffuse white light (3,000 lx). Twenty-four h dark-adaption after light exposure, and morphological and functional assays were performed as described in Methods. A: Hematoxylin-eosin (H&E) staining showed that the outer-plus-inner-segment and outer nuclear layers of the retina from Rdh13^−/− mice that were exposed to light obviously disintegrated. B: The thicknesses of the outer-plus-inner-segment and outer nuclear layers of all genotypes exposed to the light and the control group was valued. Values were mean±SD (n=5, each group). There were statistically significant differences in the thickness of the outer-plus-inner-segment and outer nuclear layer between the light exposed Rdh13^−/− mice and the other three groups at any distance point. C: The scotopic electroretinogram response of Rdh13^+/+ and Rdh13^−/− mice, which were recorded in all groups. D: The amplitudes of a- and b-waves in all genotypes was plotted as the mean±SD (n=5, each goup); *: p<0.05. E: Mitochondria in photoreceptor inner segments of Rdh13^+/+ and Rdh13^−/− mice exposed to the light were detected by transmission electron microscopy. Distinctly swollen mitochondria with disrupted cristae were observed in Rdh13^−/− mice (arrows). F and G: Cytochrome c (CytC) and apoptotic gene expression in all groups were analyzed by Western Blot, which revealed that levels of CytC, apoptosis proteinase activating factor-1 (Apaf-1), cleaved caspase 3, nuclear factor-kappa B P65 (p65) and B-cell lymphoma 2-associated X protein (Bax) were clearly increased in the cytoplasm of Rdh13^−/− mice; ONH, optic nerve head; RPE, retinal pigment epithelia; OS, outer segment; IS, inner segment; ONL, outer nuclear layer; OPL, outer plexiform layer; INL, inner nuclear layer; IPL, inner plexiform layer; GCL, ganglion cell layer; UV, ultraviolet.