April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Measuring Antioxidant Protection in a Rat Model of Light Induced Retinal Damage
Author Affiliations & Notes
  • D. T. Organisciak
    Petticrew Research Laboratory, Department of Biochemistry & Molecular Biology, Wright State University, Dayton, Ohio
  • R. M. Darrow
    Petticrew Research Laboratory, Department of Biochemistry & Molecular Biology, Wright State University, Dayton, Ohio
  • L. S. Barsalou
    Petticrew Research Laboratory, Department of Biochemistry & Molecular Biology, Wright State University, Dayton, Ohio
  • J. C. Lang
    Alcon Research, Ltd., Fort Worth, Texas
  • Footnotes
    Commercial Relationships  D.T. Organisciak, Alcon Research, Ltd., F; R.M. Darrow, None; L.S. Barsalou, None; J.C. Lang, Alcon Research, Ltd, E.
  • Footnotes
    Support  Research Funding Alcon Ltd. Fort Worth TX and Ohio Lions Eye Research Foundation.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 2259. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      D. T. Organisciak, R. M. Darrow, L. S. Barsalou, J. C. Lang; Measuring Antioxidant Protection in a Rat Model of Light Induced Retinal Damage. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2259.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : Antioxidants are known to reduce the extent of light-induced retinal degeneration in animal models, but comparing effectiveness is difficult. We treated rats with a variety of natural or synthetic antioxidants, at various concentrations, to determine their relative efficacy in preventing retinal light damage.

Methods: : Sprague-Dawley rats were reared in darkness for 40 days and then treated with intense green light (490-580nm; 1200 lux) for 4 hrs, beginning at 9:30 am. One hr before light, rats were treated (1X IP) with: ascorbic acid, α-tocopherol, various forms of rosemary from the plant Rosmarinus officinalis or dimethylthiourea (DMTU). Some rats were given rosemary 1 hr after the start of light. Following light treatment, rats were returned to darkness for 14 days. Photoreceptor cell loss was then determined by measuring rhodopsin and retinal DNA in light exposed and unexposed rats. For each dose of antioxidant, protective efficacy was calculated from the average recovery of rhodopsin and DNA in experimental vs.control animals. The effects of light and antioxidants on protein markers of oxidative stress, retinal heme oxygenase-1 (HO-1) and carboxyethylpyrrole (CEP) lipid-protein adducts, were determined by Western analysis.

Results: : The concentration of antioxidant required to achieve 50% efficacy in light damage was 250 and 200 mg/kg body weight for ascorbic acid and DMTU. Rosemary, in an oil extract or powder form, provided the same level of protection with 2-10 fold lower doses, α-tocopherol was ineffective. The active fractions of rosemary were 5-10% by weight, respectively, and it was most effective when given before light onset. In retinal extracts, rosemary and DMTU reduced the levels of immunoreactive HO-1 and CEP.

Conclusions: : Comparisons of antioxidant efficacy, based on rhodopsin and DNA recovery, provide a direct index of protection against light-induced retinal damage. Rosemary is more effective than other natural or synthetic antioxidants in preventing retinal light damage and appears to do so by reducing oxidative stress during light exposure.

Keywords: antioxidants • retina • retinal degenerations: cell biology 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×