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The purpose of the study by Osborne et al. (953) was to examine whether light exposure (400-760 nm) is detrimental to cultured cells, whether this effect requires alterations of the mitochondrial respiratory chain, as well as investigates whether exposure of the rat eye to a defined regimen of insult with light of a specific wave length causes biochemical changes to retinal ganglion cells (RGCs). Using immortalized fibroblasts and RGC-5 cells, this study assessed ATP level, apoptotic cell death, ROS production and mitochondrial respiratory chain activity after exposure of light (1000 lux) or treatment of various antioxidants. The authors reported that light (400-760 nm) provokes apoptosis in cultured RGC-5 cells, and that this effect is enhanced in serum deprivation, and attenuated by various oxidants. Further, light-induced apoptosis requires the participation of the mitochondrial respiratory chain. Finally, exposure of a pigmented rat to white light causes alteration of retinal mRNA expression and optic nerve proteins. In conclusion, the authors suggest that reducing the amount of light reaching the retina might be beneficial to glaucoma patients. It would be interesting to use purified primary RGC or differentiated RGC-5 cell in vitro, as well as mouse or rat experimental models, in future studies in vivo to convince the relevance to certain optic neuropathies including glaucoma and Leber's hereditary optic neuropathy. Further, in parallel with mitochondrial bio-energetic experiments, it would be helpful to show alterations of mitochondrial structure in RGC following light treatment to better understand the mechanism of light-induced mitochondrial dysfunction.