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L M Rapp, P L Fisher, H S Dhindsa; Reduced rate of rod outer segment disk synthesis in photoreceptor cells recovering from UVA light damage.. Invest. Ophthalmol. Vis. Sci. 1994;35(9):3540-3548.
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PURPOSE: Recovery of photoreceptor cells after light damage is thought to involve the physiologic process of disk renewal. However, only indirect evidence is available to support this hypothesis. The present study sought to examine more directly the mechanisms of photoreceptor cell recovery by quantitatively assessing the rate of rod outer segment (ROS) disk synthesis in retinas damaged by ultraviolet-A (UVA) light. METHODS: Pigmented rats were anesthetized, and their right eyes were exposed for 1 hour to a uniform field of UVA light at a dose of 6 J/cm2. Animals were returned to their dim cyclic light environment and were allowed to recover for various time points up to 42 days, at which time their eyes were enucleated for histologic examination and quantification of outer nuclear layer (ONL) thickness. Seven days before the 6- and 21-day time points, some animals were intravitreally injected with 3H-leucine in both eyes, and these eyes were used to analyze autoradiographically the rate of ROS disk synthesis. RESULTS: ROS disk synthesis in UVA-exposed eyes was 43% slower relative to nonexposed controls in the more severely damaged superior retina at postexposure day 6. Ultrastructural observations revealed a sharp demarcation between damaged and recovered ROS disks at this time. At postexposure day 21, there was a marked recovery in outer segment structure despite a further decrease in ONL thickness and a continued slow rate of disk synthesis. In the less severely damaged inferior region of the retina, the rate of disk synthesis was not altered by UVA exposure, although mild ROS disruption was evident at the earlier time points. CONCLUSIONS: These findings indicate that the rate of ROS disk synthesis is slowed in moderately damaged photoreceptor cells even though they eventually fully recover in structure. A slow-down of this rate after UVA exposure may be an adaptive change geared toward recovery mechanisms, or it may simply be a manifestation of cellular damage.
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