| The present study was designed to investigate the dynamics of selected macromolecules in eyes of mice of various ages, and in young mice exposed to visible-light stressors of different intensity and duration. The normally-aging group consisted of a total of 30 male and female Heterogeneous Stock (HS) mice of ages 170, 470 and 670 days. Light-stressed animals, 40 male and female HS mice of age 170 days, were exposed to one of four lighting categories: (1) 90 lux of cyclic light; (2) 90 lux of continuous light; (3) 800 lux of cyclic light; (4) 800 lux of continuous light. Eyes were removed, and quantification of corneal and lens catalase activity, retinal pigment epithelial (RPE) and choroidal melanin, and RPE acid phosphatase activity was accomplished using scanning-integrating microdensitometry. Additionally, insoluble lens protein content was measured using spectrophotometry. Results from aging eyes revealed a progressive accumulation of insoluble lens protein and enzymatic inactivation. These changes are perhaps attributable to the cumulative effects of auto- and photo-oxidation and their resultant free radical-induced damage to biomolecules. Light-stressed ocular tissue generally exhibited less measurable macromolecular change than did aged eyes. Exposure to abnormal lighting schemes induced an increase in melanin, and those mice exposed to intense continuous light exhibited loss of acid phosphatase activity within the central RPE. The young, light-stressed eye seems better equipped, via various protective features, to counteract oxidative damage than do unstressed senescent eyes, but is compromised by loss of the light/dark cycle. |
