REDUCED RATE OF ROD OUTER SEGMENT DISK SYNTHESIS IN PHOTORECEPTOR CELLS RECOVERING FROM UVA LIGHT DAMAGE

Purpose. Recovery of photoreceptor cells after light damage is thought to involve the physiologic process of disk renewal. However, only ind irect evidence is available to support this hypothesis. The present st udy sought to examine more directly the mechanisms of photoreceptor ce ll 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 e xposed for 1 hour to a uniform field of UVA light at a dose of 6 J/cm( 2). Animals were returned to their dim cyclic light environment and we re allowed to recover for various time points up to 42 days, at which time their eyes were enucleated for histologic examination and quantif ication of outer nuclear layer (ONL) thickness. Seven days before the 6- and 21-day time points, some animals were intravitreally injected w ith H-3-leucine in both eyes, and these eyes were used to analyze auto radiographically the rate of ROS disk synthesis. Results. ROS disk syn thesis in UVA-exposed eyes was 43% slower relative to nonexposed contr ols in the more severely damaged superior retina at postexposure day 6 . Ultrastructural observations revealed a sharp demarcation between da maged and recovered ROS disks at this time. At postexposure day 21, th ere 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 mod erately damaged photoreceptor cells even though they eventually fully recover in structure. A slowdown of this rate after WA exposure may be an adaptive change geared toward recovery mechanisms, or it may simpl y be a manifestation of cellular damage.