Are observations on ultraviolet (UV)- and visible light-induced ocular changes in animals relevant for human pathology? Different conclusions are drawn by different groups, depending on their perspective: while in the epidemiologist's view the evidence for those lesions is mostly limited or insufficient, laboratory scientists continually extend observations on radiation damage in animals. Consequently, there are diverging views on the necessity and specifications for eye protection. In this review, problems of epidemiological surveys and observations in humans and animal studies are discussed, and natural and artificial protection of the eye is outlined. The human and animal eye has an inherent potential for photochemical lesions due to chromophores including the visual pigments that are present at birth. Lifelong light exposure gives rise to additional absorbing molecules. With decreasing wavelengths of the electromagnetic spectrum the number of absorbing molecules rises; therefore, the likelihood of a photochemical reaction grows. As the spectral energy is augmented, more damage will occur. In our view, the knowledge gained from laboratory studies is a significant component of the total evidence from different fields-epidemiology, clinical observations, model studies and theoretical calculations-that UV radiation and short-wavelength visible light can cause acute and chronic changes in ocular structures. Such changes may comprise irreversible damage. Following recently issued recommendations of the major visual health organizations in the United States, protection against UV and blue light should be incorporated into the spectrum of safety considerations for sunglasses.

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Light exposure not only elicits a visual response but may also alter functional and structural characteristics of the retina. Furthermore, light exposure can lead to reversible or irreversible lesions of photoreceptors and pigment epithelium. Previous studies in our laboratory have shown that light liberates arachidonic acid from retinal membrane phospholipids mainly by activating the phospholipase A2. In this study we show that light and trauma elicit the synthesis of leukotriene B4 in the isolated rat retina in vitro. Male albino rats were dark adapted for 36 h, isolated retinae were taken, incubated and exposed a) either to darkness or to 5,000 lux of cool white fluorescent light for 5, 10 or 15 min at 37 degrees C, b) either to darkness or to 5,000 lux of cool white fluorescent light for 15 min at 0 degrees C or c) either to darkness or to 5,000 lux of cool white fluorescent light for 15 min at 37 degrees C with a 5-lipoxygenase inhibitor (zileuton). Eicosanoids were extracted and leukotriene B4 levels were determined by radioimmunoassay. Removal of retinae and incubation in darkness caused a significant rise in leukotriene B4 levels with increasing incubation time. This rise was further augmented significantly after light exposure. The leukotriene B4 levels obtained when incubating the retinae either at 0 degree C or with the lipoxygenase inhibitor zileuton as well as the high specificity of the radioimmunoassay indicate that the light- and trauma-elicited synthesis of leukotriene B4 is mediated by activating the 5-lipoxygenase. Leukotriene B4 may be involved, at least in part, in the pathogenesis of retinal diseases including light damage. Curr. Eye Res. 14: 1001-1008, 1995.

the glycosaminoglycan storage in pigment epithelium is reminiscent of that seen in some inherited mucopolysaccharidoses of humans. When a given cell type shows lysosomal accumulation of glycosaminoglycans as a consequence of impaired degradation, it can be assumed to be engaged in the turnover of glycosaminoglycans under normal conditions. Thus the present results suggest that not only the retinal pigment epithelium but also Müller cells, photoreceptor cells, and, to variable degree, retinal neurons are normally involved in the catabolism of sulphated glycosaminoglycans. We believe that the lysosomal storage of glycosaminoglycans caused secondary cellular disturbance responsible for the functional changes shown by electroretinography.