The retina represents a paradox, in that, while light and oxygen are essential for vision, these conditions also favour the formation of reactive oxygen species leading to photochemical damage to the retina. Such light damage seems to be multi-factorial and is dependent on the photoreactivity of a variety of chromophores (e.g., vitamin A metabolites, lipofuscin, melanin, flavins, porphyrins, carotenoids) endogenous to the retina. The aim of this article is to provide a detailed review of our current understanding of the photochemistry and photobiology of these chromophores and to consider how they may contribute to retinal ageing and pathology.

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Exposure of the eye to intense light, particularly blue light, can cause irreversible, oxygen-dependent damage to the retina. However, no key chromophores that trigger such photooxidative processes have been identified yet. We have found that illumination of human retinal pigment epithelium (RPE) cells with light induces significant uptake of oxygen that is both wavelength- and age-dependent. Analysis of photoreactivity of RPE cells and their age pigment lipofuscin indicates that the observed photoreactivity in RPE cells is primarily due to the presence of lipofuscin, which, under aerobic conditions, generates several oxygen-reactive species including singlet oxygen, superoxide anion, and hydrogen peroxide. We have also found that lipofuscin-photosensitized aerobic reactions lead to enhanced lipid peroxidation as measured by accumulation of lipid hydroperoxides and malondialdehyde in illuminated pigment granules. Hydrogen peroxide is only a minor product of aerobic photoexcitation of lipofuscin. We postulate that lipofuscin is a potential photosensitizer that may increase the risk of retinal photodamage and contribute to the development of age-related maculopathy.

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