Introduction: Ocular Photobiology¶

It is our pleasure to offer to you a rich array of papers on ocular photobiology. We define ocular photobiology as any biological process, positive or negative, that occurs in the eye and requires light. The 12 articles contained in this Symposium-in-Print represent both review articles of current literature and original research in this field. We begin with a review by David Sliney (1) of the geometry of the eye and how that geometry affects light transmission to each chamber of the eye. The human eye is exquisitely designed to protect itself from excessively intensive light, transmitting to the retina only the amount of light necessary to perform its biological functions. Sliney reminds us that this geometry must be taken into account when estimating the light needed to induce ocular damage or when defining action spectra of a particular ocular event. The visible light (400–700 nm) transmitted to the retina has two major biological functions, namely control of vision and of circadian rhythm; this has been reviewed by Roberts (2). It is essential to understand the natural process by which light impinging on the rods and cones finally results in sight if we are to determine where this process might be interrupted and lead to loss of vision. On the other hand, for our daily circadian rhythm, the most powerful modulator (zeitgeist) is long wavelength visible blue light (460–480 nm). As has been demonstrated by the authors quoted in this review, the primary photoreceptors for the circadian response are not in the rods and cones but in the retinal ganglion cells. Although light may be beneficial, as we age previously safe light levels may now damage the eye. The wavelength of light that causes damage to a particular region of the eye is determined by the transmission characteristics of the eye. The cornea filters out radiation below 295 nm (UV-C and short UV-B). Therefore it is not surprising that solar UV radiation would damage corneal epithelium cells, and this has been clearly demonstrated by Choy et al. (3) in their original research paper. The corneal epithelial cells exist in layers in their natural state in the eye. Choy et al. have been able to apply the comet assay, which measures DNA damage, to measure damage to each layer of cells. As perhaps could be expected, cells from the outermost layer contain the most DNA damage. Interestingly, UV-B radiation was found to induce more DNA strand breaks than energy-matched doses of UV-A and UVC. Furthermore, the data suggest that depletion of ascorbate (vitamin C) or thinning of the cornea may increase susceptibility to UV radiation damage. UV light not filtered by the human cornea is absorbed by chromophores in the lens with the result that the adult primate lens absorbs UV-B and UV-A. For most of life these lenticular chromophores have little or no phototoxicity; however, in disease states (diabetes in particular) or upon reaching middle age, these chromophores are modified in such a way as to become moderate-to-severe phototoxic agents. Balasubramanian (4) has reviewed the chemistry and biology of those chromophores endogenous to the lens and has described how their modification finally results is the formation of a cataract. He has also reviewed how the appropriate administration of antioxidants could help delay cataract progression. Dovrat and Sivak (5) describe a unique method (the Scan Tox) for monitoring lens optical quality in culture conditions that mimic conditions inside the eye. This system allows for the early detection of lens opacity (cataract) induced by various exogenous agents and prevention of this damage with antioxidants. Visible light and UV radiation not filtered by the cornea reach the conjunctiva and iris but not the uvea and choroid. However, recent epidemiological study demonstrated that sunlight plays a definite role in the occurrence of conjunctival melanoma and perhaps iridal melanoma but may not be a major factor in the etiology of ciliary body and choroid melanoma. The photobiology of these melanoma cells and their melanocytes is reviewed by Hu (6). Unlike the skin, the eye does not ‘‘tan’’ in response to UV light. These and other differences between dermal and uveal melanocytes are explained in this review. The paper by Liu et al. (7) describes the use of chemical degradation, imaging techniques and solid-state nuclear magnetic resonance (NMR) spectroscopy to study ocular melanosomes from bovine eyes. These authors find differences in the chemical composition of melanosomes from the choroid, iris and retinal pigment epithelium. Furthermore, within the same tissue there are significant differences between newborn and 2-year-old specimens. This study is the first to compare melanosomes from different tissues isolated from the same set of eyes and suggests that there are chemical and perhaps functional differences between melanosomes of different tissues. The origins of these differences for the uveal melanosomes are further explored by Hong and Simon (8) using X-ray photoelectron spectroscopy and infrared absorption. In the adult primate eye, the filtering characteristics of the anterior (front) segment are such that only visible light reaches the {Posted on the website on 10 May 2005 *To whom correspondence should be addressed: Department of Natural Sciences, Fordham University, Room 813, 113 West 60th Street, New York, NY 10023 E-mail: jroberts@fordham.edu 2005 American Society for Photobiology 0031-8655/05