Effect of Different Exposure Patterns of Low Intensity Blue Light on Mice Retina

Abstract

 

Purpose:

 

To evaluate retinal changes after low intensity light irradiation with different exposure patterns.

 

Methods:

 

Freely moving 2-month-old C57BL/6N mice were kept under normal environment or different patterns of low intensity blue light exposure (500Lux, 480nm), including continuous and cyclic exposure (every 1, 2 and 3 days). The eyes were enucleated at 1 and 3 months after fundus examination. Retinal damage was evaluated with morphology and TUNEL staining. Microglias were detected by immunohistochemistry with Iba-1 and CD45 and their numbers were quantified. The expression of MCP-1 was determined by enzyme linked immunosorbent assay (ELISA).

 

Results:

 

Continuous low intensity light showed obvious hazard to mice retina, as evidenced by the geographic atrophies in fundus examination and thinning of the outer nuclear layer (ONL) in morphology at both 1 and 3 months (p<0.01), while no significant ONL thinning was detected in the other groups. TUNEL positive cells were detected at the ONL of all irradiated mice, and their number in the continuous exposure group was significantly more than those in any cyclic exposure groups at 1 month (p<0.01). The number of TUNEL positive cells at 3 months was similar to that of 1 month in the cyclic exposure groups, while the positive cells significantly decreased at 3 months in the continuous exposure group (p<0.01). MCP-1 significantly increased in RPE layer in all irradiated mice (p<0.01). Activated microglia accumulated in the outer retina after light irradiation and increased in a time-dependent manner. More activated microglia invaded into the outer retina in the continuous irradiated group than the other groups (p<0.05).

 

Conclusions:

 

Low intensity blue light exposure can induce microglial activation and chronic inflammation. Continuous exposure induced substantial retinal damage even with low intensity, while cyclic exposure of low intensity blue light can induce chronic inflammation without severe retinal damage, which may contribute to establish an animal model of age-related macular degeneration.

 

Keywords: radiation damage: light/UV • apoptosis/cell death • microglia