May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Oxidative Damage Is a Potential Cause of Cone Cell Death in Retinitis Pigmentosa
Author Affiliations & Notes
  • A. Dong
    Johns Hopkins University, Baltimore, MD
  • J. Shen
    Johns Hopkins University, Baltimore, MD
  • X. Yang
    Johns Hopkins University, Baltimore, MD
  • R.M. Petters
    North Carolina State University, Raleigh, NC
  • Y.–W. Peng
    Duke University, Durham, NC
  • F. Wong
    Duke University, Durham, NC
  • P.A. Campochiaro
    Johns Hopkins University, Baltimore, MD
  • Footnotes
    Commercial Relationships  A. Dong, None; J. Shen, None; X. Yang, None; R.M. Petters, None; Y. Peng, None; F. Wong, None; P.A. Campochiaro, None.
  • Footnotes
    Support  EY05951, EY12609, and core grant P30EY1765 from the NEI
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 5232. doi:
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      A. Dong, J. Shen, X. Yang, R.M. Petters, Y.–W. Peng, F. Wong, P.A. Campochiaro; Oxidative Damage Is a Potential Cause of Cone Cell Death in Retinitis Pigmentosa . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5232.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: Retinitis pigmentosa (RP) is a prevalent cause of blindness caused by a large number of different mutations in many different genes. The mutations result in rod photoreceptor cell death, but it is unknown why cones die. This study was designed to test the hypothesis that cones die from hyperoxia–induced damage in patients with RP. Methods: Indirect immunofluorescent staining was done for four biomarkers of oxidative damage a transgenic pig model of RP in which Pro347Leu mutated rhodopsin is expressed in rod photoreceptors. Results: The presence of acrolein– and 4–hydroxynonenal–adducts on proteins is a specific indicator that lipid peroxidation has occurred, and there was strong immunofluorescent staining for both in cone inner segments of 10 month–old transgenic pigs in which almost all rods had died, compared to faint staining in 10 month–old control pig retinas. In 22 month–old transgenic pigs in which all rods and many cones had died, staining was strong in cone axons and some cell bodies as well as inner segments indicating progression in oxidative damage between 10 and 22 months. There was also progressive increased staining for nitrotyrosine and 8–OH–deoxyguanosine, biomarkers for oxidative damage to proteins and DNA, respectively. Conclusions: These data support the hypothesis that death of rods results in decreased oxygen consumption and hyperoxia in the outer retina resulting in gradual cone cell death from oxidative damage.

Keywords: oxidation/oxidative or free radical damage • retinitis • immunohistochemistry 

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