Failure of vitamin E to protect the retina against damage resulting from bright cyclic light exposure.

Cumulative light-mediated damage to the retina over a long time period may be involved in the development of age-related retinopathies. Light is thought to produce retinal damage by initiating autoxidative reactions among the molecular components of the retina. Experiments were therefore conducted (1) to confirm that long-term differences in cyclic light intensity affect the rate of age-related photoreceptor cell loss from the retina; and (2) to determine whether the antioxidant, vitamin E, is an effective inhibitor of damage to the retina by bright cyclic light. Albino rats were fed a basal diet either supplemented with or deficient in vitamin E. Each dietary group was divided into two light-treatment groups which were exposed to 12 hr cyclic light of either 15 lux or 750 lux. After 10 and 17 weeks of treatment, retinal photoreceptor cell densities were determined for animals in each group. Vitamin E deficiency resulted in moderate decreases in photoreceptor cell densities in the dim-light groups after both 10 and 17 weeks. Rats exposed to the bright-light condition suffered a pronounced loss of photoreceptor cells by 10 weeks, and an even greater cell loss by 17 weeks. Vitamin E deficiency did not enhance the effect of bright cyclic light in reducing photoreceptor cell densities. Thus, it appears unlikely that retinal damage by cyclic light occurs via an autoxidative mechanism.