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R. Hera, C. Puech, M. Mauget-Faysse, X. Leverve, H. Roth, C. Chiquet, J. Romanet; Superoxyde Dismutase in Antioxydant Treatment of Armd. Invest. Ophthalmol. Vis. Sci. 2009;50(13):258.
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to evaluate the protective effect of SOD on the ARMD bilateralization.Acting directly on the anti-radical enzyme chain, the superoxide dismutase (SOD), a major enzyme of the anti-oxidant system, provides an alternative of the antioxidants treatment in ARMD. Its synthesis depends on the cellular oxygenated reactive species, and leads to the conversion of the superoxide ion (O2-) into hydrogen peroxide (H2O2). This compound is the cell watch guard continuously regulating a free radicals’ detoxifying chain. Subsequently, by increasing the production of H2O2, the administration of SOD can trigger endogenous antioxidant mechanisms.
Population: 42 subjects treated in two study groups:Group A = sham, n = 22 patients; Group B = SOD, n = 20 patients.Evolution Month 0 / Month 24:Neovascularisation: 28% for Group A vs. 32% for Group B, insignificant difference between the two groups.Comparison on AREDS scale: all the patients are getting worse. We find at two years a significant difference between the two groups in favor of goup A.
In our study, oral administration of SOD doesn’t protect against the onset of neovascular ARMD in the second eye.The significance of the data must be mediated by the lack of statistic relevance of the results ( small number of patients,only two years of follow up). We can assume also that SOD administration triggers a ramp up of the antioxidant chain, and that requires the participation of other enzymes (gluthation peroxidase Gpx and catalase) for a complete detoxifying of the free radicals generated by the enzyme chain. Some of those, such as the hydroxyl radical (OH.), can be more damaging than the original O2- .As previously shown in POLA study Gpx is maybe already working at full capacity in ARMD, and can’t accommodate anymore the increased activity required by SOD administration.
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