May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Retinal Damage Caused by White Fluorescent Light in Rats Is Not Altered by Ultraviolet Cut–Off Filter
Author Affiliations & Notes
  • S. Kaidzu
    Department of Ophthalmology, Shimane University School of Medicine, Izumo, Japan
  • H. Masuda
    Department of Ophthalmology, Shimane University School of Medicine, Izumo, Japan
  • M. Tanito
    Department of Ophthalmology, Shimane University School of Medicine, Izumo, Japan
    Departments of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, OK
  • A. Ohira
    Department of Ophthalmology, Shimane University School of Medicine, Izumo, Japan
  • Footnotes
    Commercial Relationships  S. Kaidzu, None; H. Masuda, None; M. Tanito, None; A. Ohira, None.
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 2895. doi:
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      S. Kaidzu, H. Masuda, M. Tanito, A. Ohira; Retinal Damage Caused by White Fluorescent Light in Rats Is Not Altered by Ultraviolet Cut–Off Filter . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2895.

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

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Abstract

Purpose: : Intense light exposure to rodent eyes has been used as an experimental model of retinal degeneration. In this model, visible wavelengths of light are generally thought to elicit the retinal damage. However, white fluorescent bulbs, which are frequently used as a light source, radiate a broad spectrum of light including ultraviolet (UV) A, UVB, and visible light. Since rodent crystalline lenses transmit both UVA and visible light, UVA may also cause retinal degeneration in this model. We tested whether UVA is involved in the mechanism of retinal degeneration induced by white light exposure in rats.

Methods: : Sprague–Dawley rats (5–week–old, male) were exposed to white fluorescent light (FL45W, Matsushita Electric Industrial Co. LTD) at 3000 lux for 24 h. In some rats, the same intensity of damaging light was exposed through a UV cut–off filter (PC–SMK, Yamamoto Kogaku Co., LTD). Retinal damage was assessed by measurement of outer nuclear layer (ONL) thickness 24h and 7 days after light exposure. Photoreceptor cell apoptosis was analyzed by TdT–mediated dUTP nick endlabeling (TUNEL) staining 24 h after exposure. Levels of 8–hydroxy–deoxyguanosine (8–OHdG), a marker for oxidized DNA, were measured by immunostaining of retinal sections 24hours and 7 days after light exposure.

Results: : After light exposure, ONL thickness was decreased in both filter (–) and (+) groups and was not significantly different at any retinal location (14 data points) (p>0.05). Both the number of TUNEL–positive cells in the ONL and the level of 8–OHdG in the ONL and retinal pigment epithelial layer increased after light exposure but there was no difference in either measure between filter (–) and (+) groups.

Conclusions: : In this model of light–induced retinal degeneration, visible light, but not UV, is the major cause of retinal damage.

Keywords: oxidation/oxidative or free radical damage • retina • retinal pigment epithelium 
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