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K. Renganathan, M. Sun, R. Darrow, L. Shan, X. Gu, R.G. Salomon, S. Hazen, D. Organisciak, J.W. Crabb; Light Induced Protein Modifications and Lipid Oxidation Products in Rat Retina . Invest. Ophthalmol. Vis. Sci. 2003;44(13):5129.
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Purpose: To better understand the mechanisms of oxidative damage in retinal pathology, we have sought the identity of lipid oxidation products and protein adducts in rat retina after in vivo exposure to damaging light Methods: Albino rats maintained in a dark environment for 2 months were exposed to intense green light (1500 lux) for 1 or 4 hours and sacrificed immediately following light treatment. Retinas were isolated and immediately protected with antioxidants. Lipids were extracted with chloroform/methanol and analyzed by LC MS. Proteins were extracted with SDS-PAGE sample buffer and analyzed by Western blotting. Results: Lipid oxidation products in rat retina from docosahexaenoyl phosphatidylcholine (DHA-PC), arachidonoyl (AA)-PC, and linoleyl (LA)-PC were more abundant after 4 h of light exposure than after 1h or no light. Anti-carboxyethylpyrrole, anti-argpyrimidine and anti-nitrotyrosine immunreactivities were significantly greater after 4h light exposure compared with control animals maintained in the dark. Anti-opsin immunoreactivity was also significantly greater after light treatment. Conclusions: Current results are consistent with our recent observation that light modulates protein nitration in rat retina (2002 Mol. & Cell. Proteomics 1, 293). Intense light also generates lipid oxidation products in rat retina in vivo that result in oxidative protein modifications such as carboxyethylpyrrole from DHA containing lipids. Argpyrimidine, derived from methylglyoxal, appears to be another protein modification induced by light. The apparent increase in opsin after light may be due to modifications that increase the solubility and extractability of this integral membrane protein. These findings justify further consideration of lipid oxidation products and protein modifications as mediators in the light-induced biochemical sequel leading to photoreceptor cell death.
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