title: Retinal light damage in rats exposed to intermittent light. Comparison with continuous light exposure.
abstract: Visible light-induced photoreceptor cell damage resulting from exposure to multiple intermittent light-dark periods was compared with damage resulting from continuous light in albino rats maintained in a weak cyclic-light environment or in darkness before light treatment. The time course of retinal damage was determined by correlative measurements of rhodopsin and visual cell DNA at various times after light exposure, and by histopathological evaluation. The effect of intense light exposures on rhodopsin regeneration and on the level of rod outer segment docosahexaenoic acid was also determined. For rats previously maintained in weak cyclic light, 50% visual cell loss was measured 2 weeks after 12 1 hr light/2 hr dark periods, or following 24 hr of continuous light. A comparable 50% loss of visual cells was found in dark-reared rats after only 5 hr of continuous illumination or 2-3 hr of intermittent light. As judged by histology, cyclic-light-reared rats incurred less retinal pigment epithelial cell damage than dark-reared animals. In both experimental rat models intermittent light exposure resulted in greater visual cell damage than continuous exposure. Visual cell damage from intermittent light was found to depend on the duration of light exposure and on the number of light doses administered. Measurements of rhodopsin and DNA 2 hr and 2 weeks after light exposure of up to 8 hr duration revealed that visual cell loss occurs largely during the 2 week dark period following light treatment. The loss of docosahexaenoic acid from rod outer segments was also greater in rats exposed to intermittent light than in animals treated with continuous light. It is concluded that intermittent light exposure exacerbates Type I light damage in rats (involving the retina and retinal pigment epithelium) and the schedule of intense light exposure is a determinant of visual cell death.
authors.affiliation: Department of Biochemistry, School of Medicine, Wright State University Dayton, Ohio 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: M
authors.initials: M
authors.lastname: Pickford
authors.forename: J C
authors.initials: JC
authors.lastname: Blanks
mesh_terms: D000818:Animals; D004247:DNA / Q000378:metabolism; D003624:Darkness; D004307:Dose-Response Relationship, Radiation; D005227:Fatty Acids / Q000378:metabolism; D008027:Light / Q000009:adverse effects*; D008297:Male; D051381:Rats; D012038:Regeneration; D012160:Retina / Q000293:injuries* / Q000378:metabolism / Q000473:pathology; D012243:Rhodopsin / Q000378:metabolism; D012374:Rod Cell Outer Segment / Q000378:metabolism; D013997:Time Factors
chemical_list: D005227:Fatty Acids; D004247:DNA; D012243:Rhodopsin