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Oxidative Damage and Responses in Retinal Nuclei Arising from Intense Light Exposure

  • D. T. Organisciak
  • R. K. Kutty
  • M. Leffak
  • P. Wong
  • S. Messing
  • B. Wiggert
  • R. M. Darrow
  • G. J. Chader

Abstract

Prolonged or high intensity visible light exposure leads to photoreceptor cell damage and loss by incompletely understood mechanisms. In the rat retina, the sequence of events associated with intense light damage is triggered by the bleaching of rhodopsin (1), and the extent of damage is modulated by other photoreceptor cell proteins involved in visual transduction (2). Thus, environmental light-rearing conditions that alter the steady state levels of rhodopsin, α-transducin and s-antigen (arrestin) can affect the ultimate fate of visual cells (2,3). However, irrespective of their prior light-rearing environment, when rats are pretreated with natural or synthetic antioxidants, retinal light damage is less than in unsupplemented animals (4–8). This indicates that intense light exposure also results in oxidative reactions within the photoreceptor cell.

Keywords

Light Exposure Light Treatment Photoreceptor Cell Opsin Gene Visual Cell 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Noell WK, Walker VS, Kang BS, Berman S. Retinal damage by light in rats. Invest Ophthalmol 1966; 5: 450–473.PubMedGoogle Scholar
  2. 2.
    Organisciak DT, Xie A, Wang HM, Jiang YL, Darrow RM, Donoso LA. Adaptive changes in visual cell transduction protein levels: Effect of light. Exp Eye Res. 1991; 53: 773–779.PubMedCrossRefGoogle Scholar
  3. 3.
    Penn JS, Thum LA. A comparison of the retinal effects of light damage and high illuminance light history. In: Hollyfield JG, Anderson RE, LaVail MM, eds. Degenerative Retinal Disorders: Clinical and Laboratory Investigations. New York: Alan R Liss; 1987: 425–438.Google Scholar
  4. 4.
    Organisciak DT, Wang HM, Li ZY, Tso MOM. The protective effect of ascorbate in retinal light damage of rats. Invest Ophthalmol Vis Sci. 1985; 26: 1580–1588.PubMedGoogle Scholar
  5. 5.
    Li ZY, Tso MOM, Wang HM, Organisciak DT. Amelioration of photic injury in rat retina by ascorbic acid: A histopathologic study. Invest Ophthalmol Vis Sci. 1985; 26: 1589–1598.PubMedGoogle Scholar
  6. 6.
    Lam S, Tso MOM, Gurne DH. Amelioration of retinal photic injury in albino rats by dimethylthiourea. Arch Ophthalmol. 1990; 108: 1751–1757.PubMedCrossRefGoogle Scholar
  7. 7.
    Organisciak DT, Jiang YL, Wang HM, Bicknell I. The protective effect of ascorbic acid in retinal light damage of rats exposed to intermittent light. Invest Ophthalmol Vis Sci. 1990; 31: 1195–1202.PubMedGoogle Scholar
  8. 8.
    Organisciak DT, Darrow RM, Jiang YL, Marak GE, Blanks JC. Protection by dimethylthiourea against retinal light damage. Invest Ophthalmol Vis Sci. 1992; 33: 1599–1609.PubMedGoogle Scholar
  9. 9.
    Kuwabara T, Funahashi M. Light effect on the synaptic organ of the rat. Invest. Ophthalmol. Vis. Sci. 1976; 15: 407–411.Google Scholar
  10. 10.
    Shahinfar S, Edward DP, Tso MOM. A pathologic study of photoreceptor cell death in retinal photic injury. Curr Eye Res. 1991; 10: 47–59.PubMedCrossRefGoogle Scholar
  11. 11.
    Messing SL, Darrow R, Leffak M., Fleischman D, Organisciak DT. Visible light-induced damage to retinal DNA in vivo. Invest. Ophthalmol. Vis. Sci. 1994; 35: 2138.Google Scholar
  12. 12.
    Kutty RK, Kutty G, Wiggert B, Chader GJ, Darrow RM, Organisciak DT. Induction of heme oxygenase-1 in the retina by intense light: Suppression by the antioxidant dimethylthiourea. Proc Nat Acad Sci. USA 1995; 92: 1177–1181.PubMedCentralPubMedCrossRefGoogle Scholar
  13. 13.
    Wong P, Kutty RK, Darrow RM, Shivaram S, Kutty G, Fletcher RT, Wiggert B, Chader G, Organisciak DT. Changes in TRPM-2/Clusterin expression associated with light induced retinal damage in rats. Biochem Cell Biology (in press).Google Scholar
  14. 14.
    Delmelle M, Noell WK, Organisciak DT. Hereditary retinal dystrophy in the rat: Rhodopsin, retinol and vitamin A deficiency. Exp Eye Res. 1975; 21: 369–380.PubMedCrossRefGoogle Scholar
  15. 15.
    Organisciak DT, Wang HM, Kou AL. Rod outer segment lipid opsin ratios in the developing normal and retinal dystrophic rat. Exp Eye Res. 1982; 34: 401–412.PubMedCrossRefGoogle Scholar
  16. 16.
    Maniatis T, Fritsch EF, and Sambrook J. (1982). Molecular Cloning: A Laboratory Manual (Cold Spring Harbor, New York: Cold Spring Harbor Laboratory).Google Scholar
  17. 17.
    Shibahara S, Muller R, Taguchi H, and Yoshida T. (1985) Cloning and expression of cDNA for rat heme oxygenase. Proc Natl Acad Sci USA, 82, 7865–7869.PubMedCentralPubMedCrossRefGoogle Scholar
  18. 18.
    Wong P, Pineault J, Lakins V, Taillefer D, Leger JG, Wang C., Tenniswood MP. Genomic organization and expression of the rat TRPM-2 (clusterin) gene, a gene implicated in apoptosis. J Biol. Chem. 1993; 268: 5021–5031.PubMedGoogle Scholar
  19. 19.
    Feinberg A.P. and Vogelstein B. A technique for radiolabeling DNA restriction endonuclease fragments to high specific activity. Anal Biochem. 1983; 132, 6–13.PubMedCrossRefGoogle Scholar
  20. 20.
    Claycamp G. Phenol sensitization of DNA to subsequent oxidative damage in 8-hydroxyguanine assays. Carcinogenesis 1991; 13: 1289–1292.CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • D. T. Organisciak
    • 1
  • R. K. Kutty
    • 2
  • M. Leffak
    • 1
  • P. Wong
    • 2
  • S. Messing
    • 1
  • B. Wiggert
    • 2
  • R. M. Darrow
    • 1
  • G. J. Chader
    • 2
  1. 1.Department of Biochemistry and Molecular BiologyWright State UniversityDaytonUSA
  2. 2.Laboratory of Retinal Cell and Molecular BiologyNational Eye Institute, NIHBethesdaUSA

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