Lincoln D T, Dashti H
Department of Ophthalmology, University of Lübeck, Germany.
Nutrition. 1995 Sep-Oct;11(5 Suppl):576-81.
A recessive gene defect leads to gradual loss of photoreceptor cells in the retinas of a rat strain developed by the Royal College of Surgeons (RCS). Previous evidence suggested that retinal degeneration in RCS rats is partly due to instability of the lysosomal membranes of the retinal pigment epithelium (RPE). Lipid peroxidation contributes to instability of lysosomal membranes. In this study, administration of the antioxidant vitamin E retarded the degenerative process in RCS rat retinas as evidenced by light- and transmission-electron microscopic examination. Photoreceptor cells as well as the RPE were in better condition in animals treated with 100 or 150 mg vitamin E/kg body weight daily than in untreated animals or animals treated with lower doses. This assertion is based on the increased survival of photoreceptor cell nuclei as evidenced by the thickness of the outer nuclear layer coupled with a reduction in the number of pycnotic nuclei, the conservation of the outer limiting membrane, and the presence of phagosome-like structures in the RPE. These and previous results in this strain of rats lead us to propose that lipid peroxidation plays an important role in the pathogenesis of this degenerative process of the retina.