Bright cyclic rearing protects albino mouse retina against acute light-induced apoptosis

Previous studies have shown that albino rats born and raised in bright cyclic light are protected from light-induced apoptosis. The present study was designed to determine if bright cyclic rearing provides protection against retinal degeneration caused by acute light exposure in albino mice.

BALB/c mice were born in dim cyclic light (5 lux, 12 h ON/OFF). At 1 week of age, half of the litters were moved into 400 lux cyclic light. At 5 weeks of age, mice raised in the dim or bright cyclic conditions were divided into two groups. One group was placed in constant light (3,000 lux for 72 h) and the other was maintained in its original cyclic light environment. Control and constant light-stressed mice were dark-adapted for 24 and 48 h, respectively, after which their eyes were removed immediately for morphologic evaluation or preparation of rod outer segment (ROS) membranes. ROS lipids were extracted and fatty acid methyl esters were analyzed by gas-liquid chromatography. Eyes used for TUNEL (terminal deoxynucleotidyl transferase mediated dUTP nick end labeling) and DNA fragmentation assays were enucleated immediately after the 72 h light exposure.

Measurement of outer nuclear layer (ONL) thickness indicated there was no difference in the number of viable photoreceptor cells in the dim-reared controls compared to bright-reared controls. Constant light exposure significantly reduced the ONL thickness in dim- and bright-reared groups, with the largest change occurring in the dim-reared mice. TUNEL assay showed no apoptotic photoreceptor cells in either control group; however, apoptotic nuclei could be detected in both exposed groups, with the largest number found in the dim-reared mice. After light exposure, DNA fragmentation was prominent in dim-reared mice, but was not present in bright-reared animals. There was no significant difference in the fatty acid composition of ROS membranes in the dim- and bright-reared control mice. However, constant light exposure resulted in a greater loss of docosahexaenoic acid (22:6n-3) in the ROS of dim-reared animals.

Mice raised in a bright cyclic light environment are protected against light-induced apoptosis. We suggest that the protection is due to the up-regulation of cell survival pathways or the down-regulation of pathways that are vulnerable to acute cell stress.