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Photoreceptor cells receive light and transduce it to electrical signals for visual perception. However, excessive exposure to visible light causes photoreceptor cells to undergo apoptosis, which is called photo-damage. This damage involves several biochemical events, including the accumulation of oxidative stress and the elevation of intracellular calcium and nitric oxide (NO). Photo-damage is thought to be related to the progression of retinitis pigmentosa and age-related macular degeneration. Therefore, understanding the molecular mechanisms of retinal photodamage using model animals may lead to new therapeutic approaches for preventing the progression of these ocular diseases. In this review, we summarize previous reports examining the mechanisms of light-induced retinal damage, and briefly describe the interventional effect of lutein against photo-damage in mice. Lutein is taken from food and systemically delivered to the retina, skin, and certain organs and tissues. It reduces the level of reactive oxygen species and acts as an anti-oxidant in the retina of light-exposed mice, ultimately preventing light-induced DNA double-strand breaks and apoptosis. Although further study is required, lutein may be proposed as a new therapeutic approach for preventing photo-damage in humans. Rec.3/29/2012, Acc.5/17/2012, pp208-212

Photo-damage mechanisms and anti-apoptotic effect of lutein in the mouse retina