April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Rod photopigment kinetics after disruption of the retinal pigment epithelium with visible light exposure
Author Affiliations & Notes
  • Benjamin D Masella
    The Institute of Optics, University of Rochester, Rochester, NY
    Center for Visual Science, University of Rochester, Rochester, NY
  • Jennifer J Hunter
    Center for Visual Science, University of Rochester, Rochester, NY
    Flaum Eye Institute, University of Rochester, Rochester, NY
  • David R Williams
    The Institute of Optics, University of Rochester, Rochester, NY
    Center for Visual Science, University of Rochester, Rochester, NY
  • Footnotes
    Commercial Relationships Benjamin Masella, Canon, Inc. (F); Jennifer Hunter, Canon, Inc. (F), Polgenix, Inc. (F), University of Rochester (P); David Williams, Canon, Inc. (F), Pfizer (C), Pfizer (R), Polgenix, Inc. (F), University of Rochester (P)
  • Footnotes
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Investigative Ophthalmology & Visual Science April 2014, Vol.55, 1651. doi:
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    • Get Citation

      Benjamin D Masella, Jennifer J Hunter, David R Williams; Rod photopigment kinetics after disruption of the retinal pigment epithelium with visible light exposure. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1651.

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

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Abstract

Purpose: Advances in high-resolution retinal imaging have led to the discovery of long-lasting retinal changes, including disruption of the RPE caused by light exposures below published safety limits (Morgan et al, 2008). To investigate the functional consequences of RPE disruption, we combined adaptive optics ophthalmoscopy with rhodopsin densitometry.

Methods: An adaptive optics scanning light ophthalmoscope (AOSLO) was modified to measure the apparent density of rhodopsin in two macaque monkeys. Before and 2 weeks after 4 different 568 nm retinal radiant exposures (RREs, 400 - 3200 J/cm2), the apparent density and regeneration rate of rhodopsin were measured. At each of 16 retinal locations, two videos were recorded simultaneously using IR (790 nm Δ17 nm) and visible (514 nm) illumination. The IR channel was used to track the retinal location while photopigment bleaching and density measurements were accomplished by modulating the intensity of the visible source. Additionally, OCT was used to measure the length of the photoreceptor outer segments before and after RPE disruption.

Results: All RREs caused visible RPE disruption. Apparent rhodopsin density was significantly reduced following 1600 J/cm2 (p=0.01) and 3200 J/cm2 (p=0.007) exposures. No significant change in apparent density was observed in response to 800 J/cm2 (p=0.36). Surprisingly, exposure to 400 J/cm2 showed a significant increase in apparent density (p=0.047). No RRE caused a measurable change in rhodopsin recovery rate. OCT measurements showed a significant decrease in the optical path length through the photoreceptor outer segments in retinal areas exposed to 800 J/cm2 and above (p<0.001).

Conclusions: At higher RREs the optical path length through the outer segments was reduced, however our results suggest that the visual cycle remained active with its rate unchanged. At the lowest exposure levels, RPE disruption was not accompanied by a loss of rhodopsin density. While it is advisable to avoid visible light exposures that may cause RPE disruption, such exposures may not necessarily be associated with a loss of visual function.

Keywords: 648 photoreceptors • 670 radiation damage: light/UV • 701 retinal pigment epithelium  
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