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A. Dong, M. Krause, H. Akiyama, J. Shen, L. Lu, S. Hackett, L. Hong, P.A. Campochiaro; SOD1, but Not SOD3, Protects Against Retinal Degeneration Induced by Paraquat or Hyperoxia . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5883.
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Superoxide dismutase (SOD) 1 and SOD3 are two important components of the oxidative defense system. In this study, we sought to determine their roles in protection against two types of oxidative stress in the retina.
Paraquat is a generator of reactive oxygen species (ROS) and causes retinal degeneration when injected into the vitreous. Exposure to hyperoxia for prolonged periods of time also causes retinal degeneration from oxidative damage. The effect of these two types of oxidative stress was investigated in mice deficient in SOD1 or SOD3 and mice that overexpress SOD1 or SOD3. Outcome measures were ERG a– and b–wave amplitudes, outer nuclear layer (ONL) thickness, inner nuclear layer (INL) thickness, and biomarkers for oxidative damage.
Compared to SOD+/+ or SOD+/– littermates, SOD1–/– mice showed significantly reduced ERG a– and b–wave amplitudes (100% and 60% reduction for 0.75 and 0.25 mM doses, respectively), greater staining for markers of oxidative damage, greater numbers of TUNEL–stained cells, and significantly reduced ONL and INL thickness after intravitreous injection of paraquat. Transgenic mice that overexpress SOD1 showed half the reduction in ERG a– and b–wave amplitudes compared to controls (extinguished ERG) one day after injection of paraquat and no reduction in ERG amplitudes compared to a 60% reduction after 4 weeks of exposure to hyperoxia. In contrast, compared to littermate controls, mice deficient in or overexpressing SOD3 were equally susceptible to paraquat–induced or hyperoxia–induced retinal degeneration.
These data suggest that SOD1, but not SOD3, protects retinal cells against retinal degeneration from oxidative stress induced by paraquat or hyperoxia. This suggests that SOD1 is an important component of the oxidative defense system in the retina and may have therapeutic potential in diseases in which oxidative damage has been implicated, such as age–related macular degeneration and cone cell death in retinitis pigmentosa.
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