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

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 thi...

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Veröffentlicht in:Experimental eye research 1999-06, Vol.68 (6), p.757-764
Hauptverfasser: RAPP, LAURENCE M, GHALAYINI, ABBOUD J
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description 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.
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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. 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Visual pathways and centers. Vision</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>light damage</topic><topic>photoreceptor cell</topic><topic>Radiation Injuries, Experimental - metabolism</topic><topic>Radiation Injuries, Experimental - pathology</topic><topic>Rats</topic><topic>Rats, Long-Evans</topic><topic>Rhodopsin - metabolism</topic><topic>Rhodopsin - radiation effects</topic><topic>rhodopsin, opsin, regeneration</topic><topic>Rod Cell Outer Segment - metabolism</topic><topic>Rod Cell Outer Segment - pathology</topic><topic>Rod Cell Outer Segment - radiation effects</topic><topic>Rod Opsins - biosynthesis</topic><topic>Rod Opsins - radiation effects</topic><topic>Ultraviolet Rays - adverse effects</topic><topic>ultraviolet-A light</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>RAPP, LAURENCE M</creatorcontrib><creatorcontrib>GHALAYINI, ABBOUD J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Experimental eye research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>RAPP, LAURENCE M</au><au>GHALAYINI, ABBOUD J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Influence of UVA Light Stress on Photoreceptor Cell Metabolism: Decreased Rates of Rhodopsin Regeneration and Opsin Synthesis</atitle><jtitle>Experimental eye research</jtitle><addtitle>Exp Eye Res</addtitle><date>1999-06-01</date><risdate>1999</risdate><volume>68</volume><issue>6</issue><spage>757</spage><epage>764</epage><pages>757-764</pages><issn>0014-4835</issn><eissn>1096-0007</eissn><coden>EXERA6</coden><abstract>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.</abstract><cop>London</cop><pub>Elsevier Ltd</pub><pmid>10375439</pmid><doi>10.1006/exer.1999.0662</doi><tpages>8</tpages></addata></record>
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source MEDLINE; Access via ScienceDirect (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
title Influence of UVA Light Stress on Photoreceptor Cell Metabolism: Decreased Rates of Rhodopsin Regeneration and Opsin Synthesis
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