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W Cao, F Li, JF McGinnis; Estradiol Protects Against Hydrogen Peroxide-Induced Cell Death in Cultured Retinal Neurons . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3731.
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Purpose:To examine neuroprotective effects of 17 belta-estradiol on hydrogen peroxide (H2O2)-induced cell death in primary retinal neuronal cultures. Methods:Retinas of 0-2 day old Sprague-Dawley rats were isolated and dissociated. The cells (1 ml, 1X105 cells/ml) were plated in 24-well tissue culture plates on 12-mm coverslips that had been pretreated with poly-D-lysine, and cultured in the synthetic serum-free media for 2 weeks. Estradiol, 17 beta- or 17 alpha-, was added to cultures 1 hr. prior to exposure to various concentrations of H2O2. Some cultures were also treated with tamoxifen (estrogen receptor antagonist) or LY294002 (PI 3-K inhibitor) either alone or 30 min prior to Estradiol. Cell viability was measured by 3,(4,5-dimethylthiazol-2-yl)2,5-diphenyl-tetrazolium bromide (MTT) assay. Apoptotic cell death was evaluated by the TdT-mediated digoxigenin-dUTP nick-end labeling (TUNEL) assay. Results:17 beta-estradiol, in a dose-dependent manner, significantly attenuated oxidative neuronal death induced by 24-hr exposure to H2O2. Surprisingly, 17 alpha-estradiol, which does not bind to estrogen receptors, also attenuated H2O2 induced toxicity although to a lesser extent than 17 beta-estradiol. Tamoxifen did not reverse the protection offered by 17 beta-estradiol whereas LY294002 was partially effective. Conclusion:These results indicate that 17 beta-estradiol can attenuate H2O2 toxicity in a primary retinal neuronal culture. The mechanism underlying this neuroprotective effect by 17 beta-estradiol remains to be elucidated.
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