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1 From the Department of Ophthalmology, Shinshu University School of Medicine, Matsumoto; the 2 Department of Biological Responses, Laboratory of Infection and Prevention, Institute for Virus Research, Kyoto University; and the 3 Laboratory of Food and Biodynamics, Nagoya University Faculty of Agriculture, Japan.
PURPOSE. To investigate whether lipid peroxides play a role in retinal cell death due to ischemia–reperfusion injury, whether recombinant human thioredoxin (rhTRX) treatment reduces production of lipid peroxides of the retina, and whether such treatment reduces the number of cells expressing c-Jun and cyclin D1.
METHODS. Retinal ischemia was induced in rats by increasing the intraocular pressure to 110 mm Hg for 60 minutes. After reperfusion, immunohistochemical staining for lipid peroxide, peroxynitrite, c-Jun, and cyclin D1 and propidium iodide (PI) staining were performed on retinal sections from animals treated intravenously with and without rhTRX, a free radical scavenger. Quantitative analyses of PI-, c-Jun-, and cyclin D1–positive cells were performed after the ischemic insult. Concentration of lipid peroxides in the retina was determined by the thiobarbituric acid assay.
RESULTS. Specific immunostaining for lipid peroxides was seen in the ganglion cell layer at 6 hours after reperfusion, in the inner nuclear layer at 12 hours, and in the outer nuclear layer at 48 hours. Time course studies for PI-positive cells in the three nuclear layers coincided with those of specific immunostaining for lipid peroxides. The specific immunostaining was weakened by pre- and posttreatment with 0.5 mg of rhTRX. The number of PI-, c-Jun-, and cyclin D1–positive cells and the concentration of lipid peroxides were significantly decreased by treatment with rhTRX compared with those of vehicle-treated control rats (P < 0.01).
CONCLUSIONS. Lipid peroxides formed by free radicals may play a role in neuronal cell death in retinal ischemia–reperfusion injury.
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