May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Protective Effect of Tempol From Light- Induced Retinal Degeneration in Brown- Norway Rats
Author Affiliations & Notes
  • A. D. Baryluk
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • A. Messias
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • S. Thaler
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • R. Rejdak
    1st Eye Hospital, Medical University Lublin, Lublin, Poland
  • M. Fiedorowicz
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • S. Bolz
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • T. arnowski
    1st Eye Hospital, Medical University of Lublin, Lublin, Poland
  • F. Gekeler
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • P. Grieb
    Medical Research Centre, Polish Academy of Science, Warshaw, Poland
  • E. Zrenner
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • Footnotes
    Commercial Relationships  A.D. Baryluk, None; A. Messias, None; S. Thaler, None; R. Rejdak, None; M. Fiedorowicz, None; S. Bolz, None; T. arnowski, None; F. Gekeler, None; P. Grieb, None; E. Zrenner, None.
  • Footnotes
    Support  Kerstan-Stiftung and KFG (Zr-1/17-1)
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 1690. doi:https://doi.org/
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      A. D. Baryluk, A. Messias, S. Thaler, R. Rejdak, M. Fiedorowicz, S. Bolz, T. arnowski, F. Gekeler, P. Grieb, E. Zrenner; Protective Effect of Tempol From Light- Induced Retinal Degeneration in Brown- Norway Rats. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1690. doi: https://doi.org/.

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

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Abstract

Purpose: : To investigate the protective effects of superoxide dismutase mimetic TEMPOL on functional and anatomic rescue of photoreceptors in light- induced retinal damage in Brown- Norway rats.

Methods: : 11 rats were treated with intra-peritoneal injection of TEMPOL at 100mg/kg (n=6) or saline (n=5; control group) 30 min before exposure to 2700 lux white fluorescent light for 6 hours for light damage (LD). Ganzfeld ERG was recorded at baseline, 1 and 7 days after light damage, using a Diagnosys Espion e² and ColorDome LED light stimulator. In 12 hrs-dark adapted condition stimuli of increasing luminance (6 log cd.s/m² range) were applied to derivate the parameters of the Naka-Rushton function: Vmax: saturated dark adapted b-wave amplitude and k: luminance to reach 50% of Vmax (sensitivity). A paired flash paradigm (3 and 30 cd.s/m² - 100 to 4000 ms apart) was applied to evaluate the fast dynamics of rod desensitization. Photopic responses were recorded after 5 minutes of light adaptation (white light 25 cd/m²) with single flash and 20 Hz flicker.

Results: : Intra individual ratio of dark adapted b-wave amplitude analysis showed at 1st day after LD a reduction of Vmax to 19%±5% in control group, but a smaller reduction was seen in group treated with TEMPOL with 82%±36% of baseline.Vmax was decreased at 7th day to 11%±3% and 56%±20% of baseline in control and TEMPOL treated group, respectively. Parameter k was increased by 0,25 log cd.s/m² in control group and was -3,2±0,1 cd.s/m² in group treated with TEMPOL. Cones b-wave amplitude was reduced to 22%±10% and 70%±29% of baseline in control group and TEMPOL treated group, respectively and was kept at 10%±5% and 55%±23% of baseline 7 days after LD. Fast recovery after rod desensitization was abolished after LD in control group and showed no statistically significant reduction (p>0.05) in group treated with TEMPOL.

Conclusions: : Tempol was shown to have a protective effect on rod and cone pathways from light- induced photoreceptor degeneration in pigmented rats. Despite a partial protection (approximately 60% in Vmax), our ERG results indicate that the surviving photoreceptors have normal dark adapted sensitivity and normal recovery after short desensitization.

Keywords: photoreceptors • neuroprotection • electroretinography: non-clinical 
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