Abstract. Age-related macular degeneration (AMD) is the leading cause of blind registration in the developed world, and yet its pathogenesis remains poorly understood. Oxidative stress, which refers to cellular damage caused by reactive oxygen intermediates (ROI), has been implicated in many disease processes, especially age-related disorders. ROIs include free radicals, hydrogen peroxide, and singlet oxygen, and they are often the byproducts of oxygen metabolism. The retina is particularly susceptible to oxidative stress because of its high consumption of oxygen, its high proportion of polyunsaturated fatty acids, and its exposure to visible light. In vitro studies have consistently shown that photochemical retinal injury is attributable to oxidative stress and that the antioxidant vitamins A, C, and E protect against this type of injury. Furthermore, there is strong evidence suggesting that lipofuscin is derived, at least in part, from oxidatively damaged photoreceptor outer segments and that it is itself a photoreactive substance. However, the relationships between dietary and serum levels of the antioxidant vitamins and age-related macular disease are less clear, although a protective effect of high plasma concentrations of ␣ -tocopherol has been convincingly demonstrated. Macular pigment is also believed to limit retinal oxidative damage by absorbing incoming blue light and/or quenching ROIs. Many putative risk-factors for AMD have been linked to a lack of macular pigment, including female gender, lens density, tobacco use, light iris color, and reduced visual sensitivity. Moreover, the Eye Disease Case-Control Study found that high plasma levels of lutein and zeaxanthin were associated with reduced risk of neovascular AMD. The concept that AMD can be attributed to cumulative oxidative stress is enticing, but remains unproven. With a view to reducing oxidative damage, the effect of nutritional antioxidant supplements on the onset and natural course of age-related macular disease is currently being evaluated. Age-related macular degeneration (AMD) is the leading cause of blind registration in the western world, 119 and its prevalence is likely to rise as a consequence of increasing longevity. 225 There is a general consensus that cumulative oxidative damage is responsible for aging, and may, therefore, play an important role in the pathogenesis of AMD. In this article, we review the literature germane to oxidative processes in the retina and examine the evidence for a causal link between oxidative stress and age-related macular degeneration.

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The apparent loss of keratocytes following overnight lens wear is an optical artefact that can be explained in terms of corneal oedema causing volumetric tissue expansion and a loss of optical clarity, which hampers keratocyte detection. These findings place the onus on researchers postulating a loss of stromal keratocytes following clinical interventions, such as contact lens wear, to account for the effects of oedema.

A compact device to derive the optical density of human macular pigment (MP) using heterochromatic flicker photometry is described. The validity of the system is assessed by measuring the optical density spectra of MP in 12 healthy subjects and comparing this with well-established previously published values. The mean spectral absorbance characteristics of MP across subjects corresponds well with accepted values. As reported in other studies, our measurements show a wide variation of MP optical densities between individuals. In our technique within-subject variability is low; standard deviations are between 0.025 and 0.15 in most cases. The overall optical density of MP ranged from 0.08 to 0.84 with a mean of 0.496 and standard deviation of 0.257 at 460 nm. The stimulus size was 0.95 degrees. The unique feature of the technique is that it allows free viewing (not Maxwellian View) of the stimulus, it can be conducted easily and quickly and does not need frequent re-calibration.