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F Li, W Cao, RE Anderson; Retinal Adaptation to Bright Cyclic Light Protects Photoreceptors From Degeneration . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1374.
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Purpose:Light history has been shown to affect the susceptibility of the albino rat retina to the damaging effects of constant light exposure. We hypothesize that this protection is probably through inhibition of apoptosis by activation and/or up-regulation of neuroprotective molecules. The purpose of the study was to further examine this possibility. Methods:Albino rat were born and raised in 5-lux cyclic light. At 8 weeks of age, animals were adapted to 400-lux cyclic light for 1, 2, 3, 4, 6, and 9 days. Light damage was then induced by exposure to constant light for 1 day at an illumination of 1700 lux. Animals were killed and their eyes removed for morphometric and biochemical analysis. TUNEL assay was used to evaluate photoreceptor cell apoptosis and Western blots were used to determine the levels of bFGF, nNOS, and caspase-3. Results:Exposure of dim-reared rats to constant light for 1 day dramatically increased TUNEL positive cells in the outer nuclear layer. Adaptation to 400 lux bright cyclic light for 4 days significantly reduced TUNEL positive cells induced by constant light exposure, which correlated with a significantly increase in bFGF expression. Interestingly, compared to control group, caspase-3 levels were not changed in constant light exposed, 400 lux adapted (4 days), or in 400 lux adapted plus constant light exposed groups. However, there was a significant increase in nNOS level in constant light exposed group. Adaptation to 400-lux bright light before constant light exposure did not affect the increase of nNOS induced by constant light, suggesting that the protection provided by adaptation may not be through nNOS. Conclusion:1) Protection of photoreceptor cells by adaptation to 400-lux bright cyclic light is due in part to up-regulation of bFGF expression. However, other as yet unidentified factors may also be involved. 2) Light- induced photoreceptor degeneration is independent of the caspase-3 pathway.
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