Abstract
Purpose: :
Exposing albino mice to bright light causes loss of retinal function, an effect partially mediated by damage caused by reactive oxygen species (ROS). Activation of NADPH oxidase by various stressors increases ROS production. The purpose of these experiments was to test whether light-induced retinal function loss is mediated by NADPH oxidase activity.
Methods: :
Balb-C mice were exposed to dim (20 lux) or bright (10,000 lux) white light for 6 hours. Mice were injected with Fulvene-5, an NADPH oxidase inhibitor, dissolved in vehicle (intralipid-DMSO) or vehicle alone. Intraperitoneal injections were given daily for two weeks. Electroretinograms (ERGs) were taken 0, 7, and 14 days following light exposure.
Results: :
Mice injected with vehicle and exposed to bright light exhibited significantly diminished ERG a-wave and b-wave amplitudes compared to mice exposed to bright light but treated with Fulvene-5 or compared to mice exposed to dim light.
Conclusions: :
Treatment with the NADPH oxidase inhibitor Fulvene-5 precluded the damaging effects of bright light exposure on retinal function as measured by ERG. It may be that bright light exposure results in activation of NADPH oxidase resulting in increased ROS production causing retinal cell damage. Retinal morphology, apoptosis, NADPH oxidase enzyme activity, redox status, and ROS content are currently being analyzed.
Keywords: neuroprotection • antioxidants • retinal degenerations: cell biology