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K. Komeima; Antioxidants Slow Cone Photoreceptor Degeneration in rd1 Mice . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5776.
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© ARVO (1962-2015); The Authors (2016-present)
In retinitis pigmentosa (RP), a large number of different mutations in many different genes result in rod photoreceptor cell death, but it is still unclear why cones die. In transgenic pigs with RP, cones show progressive staining for markers of oxidative damage after rods have died. In this study, we tested the hypothesis that after death of rods, cones die from oxidative damage.
A mixture of antioxidants was selected to try to maximize protection against oxidative damage achievable by exogenous supplements; alpha–tocopherol (200mg/kg), ascorbic acid (250mg/kg), MnTBAP (10mg/kg) and alpha–lipoic acid (100mg/kg). Mice were treated with daily injections of the mixture or each component alone between P18 and P35, the period of cone cell death. Mice were sacrificed at P35 and retinal flat mounts were stained with peanut agglutinin (PNA) to count the number of cones by confocal microscopy. Total RNA was isolated from some retinas for real time RT–PCR for rhodopsin, m–cone opsin and s–cone opsin.
The mean number of cones in each of the 4 quadrants of the retina was increased 2–fold in rd1 mice treated with the mixture of antioxidants compared to those treated with vehicle. The mixture of antioxidants also caused a 50% increase in m–cone opsin mRNA. Injection of alpha–tocopherol or alpha–lipoic acid alone, but not ascorbic acid or MnTBAP also resulted in a significant increase in cones in P35 rd1 mouse retina.
These data support the hypothesis that gradual cone cell death following rod cell death in RP is due to oxidative damage and that antioxidant therapy may provide benefit.
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