The effects of nutrition, oxidation, and other environmental factors (light intensity or darkness) on incidence and progress of posterior subcapsular opacities (PSO) associated with genetically influenced retinal degeneration are being studied in pink-eyed Royal College of Surgeons (RCS) rats, in which rod photoreceptor outer segment debris accumulates secondary to a phagocytic defect in retinal pigmented epithelium. Evidence was obtained that oxidative changes in polyunsaturated fatty acids in debris led to water-soluble toxic aldehydes, detectable in the vitreous and toxic to lens cells and membranes. Dystrophic rats fed a natural-ingredient diet (NIH-07) were highly sensitive to retina light damage, beginning at 10- to 40-lux intensity, and 27% of the rats developed mature cataracts by 7-12 months. Increased light intensity (cyclic or constant) increased the percentage of rats with mature cataracts, while dark-rearing from birth prevented PSO and mature cataracts. Rhodopsin bleaching appears essential for retina light damage and PSO. In vitro, free retinaldehyde can act as a photosensitizer to generate singlet oxygen, an extremely energetic oxidant. Our results suggest a similar effect in vivo, with damage to both lipids and proteins. Antioxidants may slow or prevent cataracts in some diseases of the human retina. A purified diet (AIN-76A) fortified with antioxidants (0.4% beta-carotene + 0.01% BHT) prevented PSO and mature cataracts in RCS rats. After a diet containing additional antioxidants (vitamin C, 1,000 mg/kg, and vitamin E, 150 mg/kg) was fed to dystrophic rats, histopathological examination showed retinal degeneration was retarded during the time the cataracts would have had their onset (23-53 postnatal days) if NIH-07 had been fed. Future studies are being directed to exploring whether retinal degeneration can be delayed further by increasing the vitamin E by a large (7-fold) factor.
