Ocular phototoxicity

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Abstract

The human eye is constantly exposed to sunlight and artificial lighting. Therefore the eye is exposed to UV-B (295–320 nm), UV-A (320–400 nm), and visible light (400–700 nm). Light is transmitted through the eye and then signals the brain directing both sight and circadian rhythm. Therefore light absorbed by the eye must be benign. Damage to the young and adult eye by intense ambient light is avoided because the eye is protected by a very efficient antioxidant system. In addition, there are protective pigments such as the kynurenines, located in the human lens, and melanin, in the uvea and retina, which absorb ambient radiation and dissipate its energy without causing damage. After middle age there is a decrease in the production of antioxidants and antioxidant enzymes. At the same time, the protective pigments are chemically modified (lenticular 3-hydroxy kynurenine pigment is enzymatically converted into the phototoxic chromophore xanthurenic acid; melanin is altered from an antioxidant to pro-oxidant) and fluorescent chromophores (lipofuscin) accumulate to concentrations high enough to produce reactive oxygen species. We have known for some time that exposure to intense artificial light and sunlight either causes or exacerbates age-related ocular diseases. We now know many of the reasons for these effects, and with this knowledge methods are being developed to interfere with these damaging processes.

Introduction

Aside from the skin, the organ most susceptible to sunlight induced damage is the eye. While light transmission through the eye is fundamental to its unique biological functions of directing vision and circadian rhythm, at the same time exposure to the intense light of the sun can pose a particular hazard: it can lead to impaired vision and, eventually, blindness. Such exposure can come with outdoor employment as well as living at low latitudes or high altitudes and/or from the reflection of light off of water, sand, or snow [1], [2], [3], [4].

The human eye is composed of several layers. The outermost layer contains the sclera, whose function is to protect the eyeball, and the cornea, which focuses incoming light onto the lens. Beneath this layer is the choroid containing the iris which is known as the uvea. This region contains melanocytes which contain the pigment melanin, whose function is to prevent light scattering. The opening in the iris, the pupil, expands and contracts to control the amount of incoming light. The iris and the lens are bathed in the aqueous humor, a fluid that maintains intraocular pressure; this fluid also contains various antioxidants. Transport to the lens is through the aqueous. The lens is positioned behind the iris. The function of the lens is to focus light onto the retina.

Behind the lens is the vitreous humor, a fluid that supports the lens and the retina and also contains antioxidants. The retina is composed of the photoreceptor cells (rods and cones) that receive light and the neural portion (ganglion, amacrine, horizontal and bipolar cells) that transduces light signals through the retina to the optic nerve. Behind the photoreceptor cells are the retinal pigment epithelial cells, Bruchs’ membrane, and the posterior choroid. The photoreceptor cells are avascular and their nutrient support (ions, fluid and metabolites) is provided by the retinal pigment epithelial cells. There is transport to the retinal pigment epithelial cells across the Bruch’s membrane by the choriocapillaris.

Section snippets

Factors that determine light damage

The effect of ambient light on the eye must be largely benign, as it serves fundamental biological functions. However, there are several conditions under which ambient light exposure becomes harmful. To determine whether light is damaging, one must consider the following factors: intensity, wavelength, site of damage, oxygen tension, chromophores, defense systems, and repair mechanisms.

Cornea

There are three ocular diseases associated with the chronic deliverance of UV-B to the cornea: photokeratitis, pingueculae and pterygia.

Conclusion

We have known for some time that exposure to intense sunlight either causes or exacerbates age-related ocular diseases. Clarification of the underlying mechanisms of induction of ocular disease has been helped by the immortalization of human corneal [10] and lens epithelial cells [13] and the establishment of pure uveal melanocyte cultures [12]. Also, it is now clear that light damage can be enhanced by certain dyes and drugs [6], and be enhanced or prevented by herbal supplements [45], [78],

Acknowledgements

The author wishes to thank Dr Ann Motten, NIEHS North Carolina, for help in preparing this paper and the Hugoton Foundation for its financial support.

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