April 2010
Volume 51, Issue 13
ARVO Annual Meeting Abstract  |   April 2010
Redox Modulation is Neuroprotective for Photoreceptor Death After Photic Injury
Author Affiliations & Notes
  • C. J. Lieven
    Ophthalmology and Visual Sciences, University of Wisconsin, Madison, Wisconsin
  • L. A. Levin
    Ophthalmology, Univ Montreal/Univ Wisconsin, Montreal, Quebec, Canada
  • Footnotes
    Commercial Relationships  C.J. Lieven, None; L.A. Levin, Wisconsin Alumni Research Foundation, P.
  • Footnotes
    Support  NIH EY R21EY017970, P30EY016665, Retina Research Foundation, Research to Prevent Blindness
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 2256. doi:
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      C. J. Lieven, L. A. Levin; Redox Modulation is Neuroprotective for Photoreceptor Death After Photic Injury. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2256.

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

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Purpose: : Light exposure is a risk factor for age-related macular degeneration and retinitis pigmentosa. Exposure to intense light in animal models of these diseases speeds the degenerative process, possibly mediated by increased oxidative stress. We previously showed that redox modulation towards a reducing environment with tris(2-carboxyethyl)phosphine (TCEP) rescues retinal ganglion cells from axonal damage in vitro and in vivo. We hypothesized that a similar therapeutic mechanism would be neuroprotective in a photic injury model of retinal degeneration.

Methods: : Male Wistar rats 6 to 10 weeks of age were reared on a 12-hour light/12-hour dark cycle. Rats were dark adapted for 16 hours, then administered TCEP (28.6 mg/kg) or saline i.p. immediately prior to exposure to uniform, omnidirectional white fluorescent light at 10 klux for 10 hrs. After exposure, rats were returned to housing for 5 days prior to sacrifice. Eyes were fixed, embedded in glycomethacrylate, sectioned at 2 microns, and stained with toluidine blue. NIH ImageJ was used to measure the thickness and area of the outer nuclear layer (ONL). Thickness measurements at regular intervals were compared by ANOVA.

Results: : Photic injury led to significant thinning of the inferior ONL (mean thickness 17.8 ± 2.9 vs. 34.3 ± 0.7 µm, p = 0.004), and nearly complete obliteration of the superior ONL (3.1 ± 0.6 vs. 37.1 ± 0.8 µm, p < 0.001 ). Pre-treatment with TCEP decreased thinning both inferiorly and superiorly (28.2 ± 4.3 and 8.0 ± 2.2 µm, respectively; p < 0.001).

Conclusions: : The systemic administration of the disulfide reducing agent TCEP decreases photoreceptor loss after photic injury. This is consistent with light-induced oxidation of certain proteins containing reduced sulfhydryls serving as a critical signal for photoreceptor death in the photic injury model. Disulfide formation in these proteins may be novel therapeutic targets in eye diseases exacerbated by light.

Keywords: photoreceptors • neuroprotection • oxidation/oxidative or free radical damage 

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