Retinitis pigmentosa / oxidative damage / Antioxidants

Antioxidants reduce cone cell death in a model of retinitis pigmentosa.
Komeima K, Rogers BS, Lu L, Campochiaro PA
Proc Natl Acad Sci U S A. 2006 Jul 25; 103(30): 11300-5

Retinitis pigmentosa (RP) is a label for a group of diseases caused by
a large number of mutations that result in rod photoreceptor cell death
followed by gradual death of cones. The mechanism of cone cell death is
uncertain. Rods are a major source of oxygen utilization in the retina
and, after rods die, the level of oxygen in the outer retina is
increased. In this study, we used the rd1 mouse model of RP to test the
hypothesis that 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
(200 mg/kg), ascorbic acid (250 mg/kg), Mn(III)tetrakis (4-benzoic
acid) porphyrin (10 mg/kg), and alpha-lipoic acid (100 mg/kg). Mice
were treated with daily injections of the mixture or each component
alone between postnatal day (P)18 and P35. Between P18 and P35, there
was an increase in two biomarkers of oxidative damage, carbonyl adducts
measured by ELISA and immunohistochemical staining for acrolein, in the
retinas of rd1 mice. The staining for acrolein in remaining cones at
P35 was eliminated in antioxidant-treated rd1 mice, confirming that the
treatment markedly reduced oxidative damage in cones; this was
accompanied by a 2-fold increase in cone cell density and a 50%
increase in medium-wavelength cone opsin mRNA. Antioxidants also caused
some preservation of cone function based upon photopic
electroretinograms. These data support the hypothesis that gradual cone
cell death after rod cell death in RP is due to oxidative damage, and
that antioxidant therapy may provide benefit.

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