Retinal Damage by Cyclic Light and the Effect of Vitamin E

Abstract

In an investigation of the mechanism by which visible light damages the retina, the role of light-induced lipid peroxidation was tested by exposing groups of rats raised on diets containing different levels of vitamin E to light for varying periods of time and analyzing their retinas morphologically. Weanling male Sprague Dawley albino rats were fed one of 3 diets differing only in their vitamin E content, exposed to 50 ft. cd. of cyclic light (12 hours on/ 12 hours off), and examined for structural alterations in the retina by light and electron microscopy. The retinas of animals fed the diet containing a normal level of vitamin E (50mg/Kg) were damaged after 4 days of light exposure, and the damage increased with increased exposure. Structural alterations were limited to the photoreceptor cells and included vesiculation of the distal halves of the outer segments, vacuole formation in the inner segments, and eventual cell death. The pattern of damage suggested the existence of more than one site of damage initiation within a given photoreceptor cell. The width of the bacillary layer and the number of nuclei in the outer nuclear layer were determined to be quantitative measures of light damage. Utilizing these measures the effects of light on the animals fed a diet containing a high level of vitamin E (250mg/Kg) and the animals fed a diet containing no vitamin E were compared. There was no difference between the groups in either measure after 4, 7, or 15 days of exposure, nor was there any difference in the ultrastructural appearance of the retina after 4 days of exposure. Results do not support the hypothesis that retinal damage by light is the result of light-induced lipid peroxidation.