The effects of nutrition, oxidation, and other environmental factors (light intensity or darkness) on the incidence and progress of posterior subcapsular opacities (PSO) associated with retinal degeneration are being studied in Royal College of Surgeons (RCS) rats, in which rod photoreceptor outer segment debris accumulates secondary to a phagocytic defect in the retinal pigmented epithelium. Evidence has been obtained that oxidative changes in polyunsaturated fatty acids in the debris lead to water-soluble toxic aldehydes that can be detected in the vitreous, and are toxic to lens membranes. Several diets have been found to prevent mature cataracts, and dark-rearing has been shown to prevent the PSO detectable miscroscopically. By exposing pink-eyed dystrophic rats to constant light of 25 footcandles beginning (1) at 20-23 postnatal days or (2) at birth, we have been able for the first time to demonstrate histopathological changes similar to those in some naturally occurring human posterior subcapsular cataracts (PSC), such as those seen in retinitis pigmentosa. Lens epithelial cells migrated to the posterior pole of the lens. Many were bizarre in shape, with abundant pale-staining cytoplasm and small (or large) nuclei (""""""""bladder cells of Wedl""""""""). Changes similar to human anterior subcapsular cataracts were also noted. RCS rats provide a readily manipulated animal model of PSC, exacerbated by some environmental factors and prevented by others. Principles established with the model may have significance for slowing or preventing human PSC.
