Reducing Oxidative Stress in Retinitis Pigmentosa Mouse Model P23H

Retinitis Pigmentosa is a genetic disorder that can disrupt our vision through the deterioration of rods cells and, eventually, cone cells. A study found that patients with RP have higher oxidative stress levels than a control group. Patients who exhibit higher levels of reactive oxygen species would not be able to adequately compensate with normal levels of antioxidant enzymes. Furthermore, previous studies have shown that SOD3 was essential for reducing the oxidative damage done to the injured tissue. Through this study, we hope to provide a method to minimize the damage done by RP and to establish the importance of the extracellular matrix in photoreceptors’ health. Transgenic heterozygous SOD3OE were crossed with a knock-in gain of function heterozygous RhoP23H/+ to produce our target genotype for this experiment, SOD3OE/RhoP23H/+. At post-natal day 30 and 60, the mice’s retinal functional ability was tested using ERG. One retina from each mouse was collected for Western blot for protein analysis, while the other was embedded in paraffin for structural analysis. The results show that the SOD3OE/RhoP23H/+ has higher ERG at P30, but not statistically significant. At P60, the ERG’s were reduced, indicating that SOD3OE cannot mitigate the effects of RhoP23H/+. The mutation overwhelms the effectivity of SOD3, and, as a result, is not a viable treatment plan for this mutation. Although the overexpression of the anti-oxidant has not entirely counteracted RhoP23H/+, this study advances the understanding of the importance of extracellular enzymes and the possibility of delaying the onset of RP in patients.