Influence of UVA Light Stress on Photoreceptor Cell Metabolism: Decreased Rates of Rhodopsin Regeneration and Opsin Synthesis

• Published in: Experimental eye research Vol. 68; no. 6; pp. 757 - 764
• Main Authors: RAPP, LAURENCE M, GHALAYINI, ABBOUD J
• Format: Journal Article
• Language: English
• Published: London Elsevier Ltd 01-06-1999; Elsevier
• Subjects: Animals; Biological and medical sciences; Electrophoresis, Polyacrylamide Gel; Eye and associated structures. Visual pathways and centers. Vision; Female; Fundamental and applied biological sciences. Psychology; light damage; photoreceptor cell; Radiation Injuries, Experimental - metabolism; Radiation Injuries, Experimental - pathology; Rats; Rats, Long-Evans; Rhodopsin - metabolism; Rhodopsin - radiation effects; rhodopsin, opsin, regeneration; Rod Cell Outer Segment - metabolism; Rod Cell Outer Segment - pathology; Rod Cell Outer Segment - radiation effects; Rod Opsins - biosynthesis; Rod Opsins - radiation effects; Ultraviolet Rays - adverse effects; ultraviolet-A light; Vertebrates: nervous system and sense organs; rhodopsin, opsin, regeneration; ultraviolet-A light; light damage; photoreceptor cell; Rhodopsin; UVA radiation; Rat; Rodentia; Photoreceptor; Retina; Biosynthesis; Metabolism; Stress; Eye; Visual system; Regeneration; Vertebrata; Mammalia; Opsin
• ISSN: 0014-4835; 1096-0007
• DOI: 10.1006/exer.1999.0662

There is considerable evidence indicating that rhodopsin is the chromophore mediating light damage to the rat retina caused by exposure to mid-visible wavelengths. Retinal damage is, however, more effectively produced by short-wavelength light, and little is known about the initiating events for this damage class. The present study sought to determine the involvement of rhodopsin bleaching in short-wavelength damage by examining rhodopsin levels and opsin synthesis at early time points following acute ultraviolet-A (UVA) exposures of the pigmented rat eye. A gradual decline in rhodopsin to 8% of the level in non-exposed control eyes occurred over a 1 hr exposure to 1500 μW cm-2of UVA light. When animals were placed in darkness following this exposure, rhodopsin had recovered to only 27% of control levels by 2 hr post-exposure indicating a very slow rate of regeneration. For later time points, animals were returned to dim cyclic light and by 2 days following exposure, rhodopsin levels had risen to 57% of control. In contrast, opsin levels at this same time point were unaffected by UVA exposure. Other observations indicating the UVA exposure affected photoreceptor cell metabolism included a 27% decrease in the rate of opsin synthesis between 1 and 2 days following exposure, and a 69% reduction in the rate of rod outer segment disk renewal during the initial 3 days following exposure.
These data show that UVA light stress in the retina causes a gradual bleaching of rhodopsin followed by a slow rate of recovery and altered photoreceptor cell metabolism. These results are consistent with the concept that rhodopsin mediates UVA-induced retinal damage and the possible mechanisms by which this might occur are discussed in relation to alternative hypotheses currently in the literature.