“Much more work needs to be done to determine if what we did in mice will work in humans,” said Peter Campochiaro, Professor of Ophthalmology at Johns Hopkins University. “But these findings have helped to solve a mystery.”
In patients with RP, rod photoreceptors die from a mutation, but it has not been known why cone photoreceptors die. After rods die, the level of oxygen in the retina goes up, and this work shows that it is the high oxygen that gradually kills the cones. Oxygen damage is also called “oxidative damage” and can be reduced by antioxidants.
In earlier studies exposing mice to pure oxygen, the Hopkins scientists found that high levels of oxygen in the retina killed both rods and cones, said Campochiaro. “This was the clue that the high oxygen levels that occur naturally in the retina after rods die was the suspect regarding cone cell death. To test this, we used antioxidants, which protect cells from oxygen damage, and since they allowed many more cones to survive, it proves that the suspect is guilty.”
In this mouse model of retinal degeneration, the rods have completely degenerated by the 18th day of age, and then the cones start to degenerate, with 85 percent of them dying off by the time the mice are 35 days old. Campochiaro and his team injected vitamin E, vitamin C, alpha-lipoic acid or an antioxidant similar to superoxide dismutase between the 18th and 35th day. In mice that received vitamin E or alpha-lipoic acid, 40 percent of the cones survived, about twice as many as in the control group or the groups treated with the other antioxidants, which had no identifiable effect.
“What’s clear is the link between oxygen and photoreceptor damage, as well as the potential of antioxidant treatment,” Campochiaro said. “These experiments suggest that an optimised regimen of antioxidants may help to protect patients with retinitis pigmentosa.”
MEDICA.de; Source: Johns Hopkins Medical Institutions