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. Retinitis pigmentosa (RP) is a genetically diverse disease, characterized by the progressive degeneration of rod and cone photoreceptors. Photoreceptor loss in RP occurs via apoptosis, a mode of programmed cell death, which allows a cell to partake in its own demise. Apoptosis therefore represents a common final pathway in the pathology of RP. However, the molecular events regulating photoreceptor apoptosis in human cases and animal models of RP remain undefined. In this study, we delineate the molecular events occurring during photoreceptor apoptosis in the light-induced retinal injury model of RP. METHODS. Retinal light damage: Adult male balb-c mice were exposed to 2 hours of cool white fluorescent light at a luminescence level of 5000 lux. Intraperitoneal injections: Mice were injected intraperitoneally with 100mgkg -1 of N G -nitro-L-arginine methyl ester (L-NAME) in phosphate buffered saline (PBS), or D-NAME (an inactive isomer) in PBS as a control, 1hr before light exposure. Flow cytometry was employed to monitor intracellular calcium levels, generation of reactive oxygen species and mitochondrial membrane depolarisation in untreated animals and in those treated with L-NAME. Caspase-3 activation was assessed by western blot and with the use of the synthetic substrate AcDEVD-pNA. The possible involvement of other caspases was assessed by treatment of the animals with ZVAD.fmk subretinally.

Light-induced Photoreceptor Apoptosis in vivo is Caspase Independent and Mediated by Nitric Oxide