May 1993
Volume 34, Issue 6
Free
Articles  |   May 1993
Bright environmental light accelerates rhodopsin depletion in retinoid-deprived rats.
Author Affiliations
  • M L Katz
    University of Missouri School of Medicine, Mason Institute of Ophthalmology, Columbia 65212.
  • H J Stientjes
    University of Missouri School of Medicine, Mason Institute of Ophthalmology, Columbia 65212.
  • C L Gao
    University of Missouri School of Medicine, Mason Institute of Ophthalmology, Columbia 65212.
  • M Norberg
    University of Missouri School of Medicine, Mason Institute of Ophthalmology, Columbia 65212.
Investigative Ophthalmology & Visual Science May 1993, Vol.34, 2000-2008. doi:
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      M L Katz, H J Stientjes, C L Gao, M Norberg; Bright environmental light accelerates rhodopsin depletion in retinoid-deprived rats.. Invest. Ophthalmol. Vis. Sci. 1993;34(6):2000-2008.

      Download citation file:


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

      ×
  • Supplements
Abstract

PURPOSE: Dietary deficiency in the retinoid precursors of the visual pigment chromophore 11-cis retinal eventually results in selective degeneration of the photoreceptor cells of the vertebrate retina. An early effect of retinoid deficiency is depletion of chromophore from the photoreceptor outer segments. Experiments were conducted to determine whether the rate of chromophore depletion was affected by the intensity of environmental light. METHODS: Rats were maintained on diets either containing or lacking retinoid precursors of 11-cis retinal for up to 30 weeks. Animals in both dietary groups were exposed to either bright (90 lux) or dim (5 lux) cyclic light for the duration of the experiment. At various time intervals retinal rhodopsin content and photoreceptor densities were determined in animals from each treatment group. RESULTS: Bright light greatly accelerated the depletion of rhodopsin from the retina. Rhodopsin was almost completely depleted from the retinas of the retinoid-deficient animals raised under bright light for 25 weeks, whereas the dim-light-reared animals fed the retinoid-deficient diet still had significant amounts of retinal rhodopsin even after 30 weeks. Bright light alone moderately depressed retinal rhodopsin levels in animals fed the diet containing a vitamin A precursor of 11-cis retinal. Among rats fed the latter diet, retinal rhodopsin content in the animals kept in bright cyclic light was maintained throughout the experiment at about 70% of the amount of rhodopsin in rats housed in dim cyclic light. The light-related rhodopsin depletion in the retinoid-deprived rats was accompanied by photoreceptor cell death. After 30 weeks of treatment, photoreceptor cell densities remained similar in all treatment groups except the retinoid-deprived group housed under bright cyclic light. In the latter group, photoreceptor cell densities in the central retinas were reduced by an average of more than 50% after 30 weeks. Retinoid deficiency and bright light exposure alone each resulted in a reduction in rod outer segment size. An even greater reduction in outer segment size was observed in vitamin A-deprived animals housed under bright cyclic light. CONCLUSION: These findings indicate that light accelerates the depletion of retinoids from the retina and the accompanying photoreceptor cell degeneration.

×
×

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.

×