Abstract
Purpose: :
Intense light initiates damage that leads to photoreceptor apoptotic cell death in albino rats. It has been shown by others that exposing rats to light prior to bright light is protective. We have shown that neuroprotectin D1 (NPD1), a derivative of DHA, attenuates apoptosis (IOVS 48:4866;2007). The purpose of this study was to determine if NPD1 may be involved in the preconditioning response.
Methods: :
Experiment 1 SD Rats were Dark-adapted for 5 days and stimulated with bright light (18kLx, 5h); retinas were collected for LC-MS-MS-based mediator lipidomic analysis. Experiment 2 Rats were light cycled 1 week (12 ON, 12 OFF); retinas were collected at various times of the day for lipidomic analysis. Experiment 3 Rats were separated into 2 groups. Both were dark-adapted for 5 days. One group was exposed to 14 hours of 700Lx light and allowed to recover for 8 hours at 15Lx prior to bright light exposure. The second group remained dark-adapted until initiation of bright light. Eyes were imaged with HRA-OCT Spectralis and collected for ONL thickness and counts. Retinas were also subjected to lipidomic analysis.
Results: :
Dark-adapted rats, exposed to increasing durations of bright light, show a time dependent increase in NPD1. NPD1 also increases (400%) with the onset of light in light cycled animals (12 ON, 12 OFF). If animals were exposed to light prior to bright light, NPD1 increases dramatically (800%) compared to animals not preconditioned. ONL counts on sections and retinal thickness by OCT show that preconditioning with 700Lx for 14h is sufficient for protection of photoreceptors exposed to intense light.
Conclusions: :
As light increases, NPD1 increases. If animals are exposed to light prior to bright light, NPD1 increases dramatically compared to those in non-preconditioned animals. This preconditioning is also protective for photoreceptors exposed to bright light. Our results suggest that NPD1 in the retina is determined by recent lighting conditions and may play a protective role in preconditioning against future light-induced oxidative stress.
Keywords: cell survival • photoreceptors • lipids