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DM Allen, WT Allison, CW Hawryshyn; Resistance to Light Damage in Albino Trout . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3734.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Studies of light damage to retinas of albino vertebrates have served as effective animal models of retinal degeneration. Previous data show that light damage in albino rainbow trout (Oncorhynchus mykiss) leads to an expected loss of rod outer segments (ROS), but in contrast to other albino vertebrates, the census of rod nuclei in the outer nuclear layer (ONL) does not change and cones do not degenerate. The aim of this study was to differentiate between two hypotheses that could account for these surprizing results: (1) rods are surviving light damage to ROS, or (2) rods are dying and being replaced by rod progenitors. Methods: Albino and normally pigmented trout were transferred into a regimen of full exposure to daylight (∼100,000 lux), or remained protected from direct sunlight(∼600 lux). Histology, TUNEL method, and immunohistochemical assay of proliferating cell nuclear antigen (PCNA) were applied to samples collected after 0,2,5,10 and 20 days of treatment. Results: ROS were maintained in pigmented fish regardless of light treatment, and in albinos protected from sunlight. Albinos in full daylight lost ROS in their central retina, and by day 20 some individuals had lost rod nuclei in a portion of their central retina. In other areas of the retina, rod nuclei were maintained in spite of ROS damage, while rods nearer to the peripheral margins maintained ROS. Cones remained intact in all retinal samples, including those in which rod nuclei had degenerated. In light-damaged albinos, pyknotic and TUNEL+ nuclei were localized to the vitread half of the ONL in the central retina; thus, areas of cell death were correlated with loss of ROS. Increased cell proliferation (PCNA+ nuclei) was present in albinos vs. pigmented fish. Conclusion: Where the ONL census is maintained in light-damaged albino trout, apoptotic demise of rods, but not cones, is apparently balanced by increased proliferation of new rods from retinal stem cells (2). However, in portions of the central retina where there is a decline in numbers of ONL nuclei, this mechanism is insuffficient to replace all degenerating rods. Protection of ROS and cell nuclei in the periphery could result from a diminished dose of light behind the iris (guanin argentea), or from growth factors in the peripheral retina exerting a protective effect. This work was supported by an Ashbel Smith Fellowship (DMA), Alzheimer Society of B.C./Canada Fellowship (WEA) and a NSERC Operating Grant (CWH).
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