ur 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 optimized regimen of antioxidants may help to protect patients with retinitis pigmentosa.’ Campochiaro emphasized that even if found valuable, antioxidant treatment of RP, a group of inherited blinding diseases with complex genetic roots, would not cure the disease.
But the salvaging of cones, which are concentrated in the retina's macula and are critical to central vision, could serve as a ‘maintenance therapy,’ he said. ‘That alone would be an enormous help.’ RP affects only about 100,000 people in the United States. But the oxygen damage has also been implicated in other more pervasive eye diseases, like AMD and cataracts. Antioxidants naturally occur in some fruits and vegetables, and are available as supplements, but Campochiaro said it remains unclear whether the amounts of antioxidants consumed in foods provided any benefit to people with these types of vision impairments.
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