title: 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.
authors.affiliation: Department of Biochemistry, School of Medicine, Wright State University, Dayton, OH 45435.
authors.forename: D T
authors.initials: DT
authors.lastname: Organisciak
authors.forename: Y L
authors.initials: YL
authors.lastname: Jiang
authors.forename: H M
authors.initials: HM
authors.lastname: Wang
authors.forename: I
authors.initials: I
authors.lastname: Bicknell
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000097:blood / Q000494:pharmacology*; D004247:DNA / Q000096:biosynthesis; D003624:Darkness; D004307:Dose-Response Relationship, Radiation; D005123:Eye / Q000378:metabolism; D008027:Light / Q000009:adverse effects*; D008297:Male; D010507:Periodicity; D010786:Photoreceptor Cells / Q000187:drug effects / Q000528:radiation effects; D011837:Radiation-Protective Agents; D051381:Rats; D011919:Rats, Inbred Strains; D012038:Regeneration; D012160:Retina / Q000187:drug effects / Q000528:radiation effects; D012164:Retinal Diseases / Q000209:etiology / Q000517:prevention & control*; D012243:Rhodopsin / Q000378:metabolism
chemical_list: D011837:Radiation-Protective Agents; D004247:DNA; D012243:Rhodopsin; D001205:Ascorbic Acid