The protective effect of ascorbic acid in retinal light damage of rats exposed to intermittent light.

Abstract

Retinal light damage in dark-reared rats supplemented with ascorbic acid and exposed to multiple doses of intermittent light was studied and compared with damage in unsupplemented dark-reared and cyclic-light-reared rats. The extent of photoreceptor cell loss from intense light exposure was determined by whole-eye rhodopsin levels and retinal DNA measurements two weeks after light treatment. Two weeks after 3 or 8 hr of intermittent light, ascorbate-supplemented animals had rhodopsin and retinal DNA levels that were two to three times higher than in unsupplemented dark-reared rats. In both types of rats rhodopsin levels were influenced by the number of light doses, the duration of light exposure, and to a lesser extent, by the length of the dark period between exposures. Rhodopsin levels in the dark-reared ascorbate-supplemented rats were significantly higher than in unsupplemented dark-reared rats, and were similar to the levels in unsupplemented cyclic-light-reared animals. Ascorbate treatment had no effect on the rate of rhodopsin bleaching. However, regeneration was greater in supplemented rats after multiple 1-hr light exposures. Intermittent light also resulted in lower ascorbate levels in the retinas of supplemented and unsupplemented rats, with dramatic losses from the retinal pigment epithelium (RPE)-choroid in both types of animals. We conclude that ascorbic acid protects the eye by reducing the irreversible Type I form of light damage in dark-reared rats. Ascorbate appears to shift light damage to the Type II form typical of cyclic-light-reared animals.