September 1992
Volume 33, Issue 10
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Articles  |   September 1992
Ascorbate treatment prevents accumulation of phagosomes in RPE in light damage.
Author Affiliations
  • J C Blanks
    Doheny Eye Institute, Los Angeles, California 90033.
  • M S Pickford
    Doheny Eye Institute, Los Angeles, California 90033.
  • D T Organisciak
    Doheny Eye Institute, Los Angeles, California 90033.
Investigative Ophthalmology & Visual Science September 1992, Vol.33, 2814-2821. doi:
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      J C Blanks, M S Pickford, D T Organisciak; Ascorbate treatment prevents accumulation of phagosomes in RPE in light damage.. Invest. Ophthalmol. Vis. Sci. 1992;33(10):2814-2821.

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Abstract

In dark-reared albino rats, exposure to 2 or 3 hr of intense light interrupted by 2 hr dark periods resulted in extensive degeneration of photoreceptor cells and degeneration of the retinal pigment epithelium (RPE). Ascorbate (ie, vitamin C) administration prior to light exposure protected photoreceptors and the RPE from light damage. In the present study, ascorbate-treated and untreated rats were exposed to various cycles of intermittent light. Immediately after this light exposure, phagosome frequency in the RPE was morphologically evaluated in comparable 50 microns sections. In untreated rats, exposure to 2 or 3 hr of intermittent light resulted in a five- to sixfold increase in phagosome density compared to unexposed controls. In contrast, no increase in phagosome density was observed in ascorbate-treated rats. In these animals, under all lighting regimens, phagosome levels remained essentially identical to those in rats not exposed to light. After a single nondamaging light exposure, phagosome density remained at the level of dark controls in ascorbate-treated and untreated rats. These results indicate that phagosome frequency may serve as an index for light damage and that the protective effect of ascorbate may be linked to its capacity to prevent rod outer segment shedding and phagocytosis under intense light conditions.

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