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F. Schuettauf, R.A. Rejdak, S. Thaler, K. Dietrich, Z. Zagorski, E. Zrenner, P. Grieb; Tempol Protects RGC Against Partial Optic Verve Crush With and Without Iron Load in the Rat . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1263.
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Purpose: Tempol (4–hydroxytetramethylpiperidine–1–oxyl), a membrane–permeable free–radical scavenger, has been shown to prevent retinal ganglion cell (RGC) degeneration in vitro. Given systemically, iron dextran was shown to produce oxidative stress in many tissues. We evaluated the effects of pre–treatment with iron dextran on RGC loss in a model of calibrated partial optic nerve crush (PONC) in rats, and on the protection offered by tempol in this experimental paradigm. Methods: Animals were pre–treated with a single iron dextran load (0.5g/kg BW i.p.) 24 hours prior to injury. Tempol (20 mg/kg BW i.p.) was given 6 hours before and daily after induction of retinal ganglion cell (RGC) loss by calibrated PONC. Control animals were treated with PBS (pH 7.2, 0.2M i.p.). RGC were retrogradely labeled with Fluorogold; all data are expressed as percent of the RGC count in the respective sham–treated eye. Results: PONC resulted in the decrease of the number of labeled RGC per square mm of retina to 31.4% after 7 days. Tempol attenuated this effect and the number of RGC spared doubled to 62.1%. In iron dextran–pretreated animals only 12.7% of the RGC remained intact after PONC, and treatment with tempol increased their number to 46.2%. Conclusions: PONC leads to significantly more pronounced RGC damage when oxidative stress is exagerrated by iron pretreatment; in this condition protection by tempol is even more efficient. Further studies are required to elucidate the mechanisms of RGC rescue.
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