Abstract
BackgroundAge-related macular degeneration (AMD) is associated with lipofuscin accumulation whereas the content of melanosomes decreases. Melanosomes are the main storage of zinc in the pigmented tissues. Since the elderly population, as the most affected group for AMD, is prone to zinc deficit, we investigated the chemical and ultrastructural effects of zinc deficiency in pigmented rat eyes after a six-month zinc penury diet.Methodology/Principal FindingsAdult Long Evans (LE) rats were investigated. The control animals were fed with a normal alimentation whereas the zinc-deficiency rats (ZD-LE) were fed with a zinc deficient diet for six months. Quantitative Energy Dispersive X-ray (EDX) microanalysis yielded the zinc mole fractions of melanosomes in the retinal pigment epithelium (RPE). The lateral resolution of the analysis was 100 nm. The zinc mole fractions of melanosomes were significantly smaller in the RPE of ZD-LE rats as compared to the LE control rats. Light, fluorescence and electron microscopy, as well as immunohistochemistry were performed. The numbers of lipofuscin granules in the RPE and of infiltrated cells (Ø>3 µm) found in the choroid were quantified. The number of lipofuscin granules significantly increased in ZD-LE as compared to control rats. Infiltrated cells bigger than 3 µm were only detected in the choroid of ZD-LE animals. Moreover, the thickness of the Bruch's membrane of ZD-LE rats varied between 0.4–3 µm and thin, rangy ED1 positive macrophages were found attached at these sites of Bruch's membrane or even inside it.Conclusions/SignificanceIn pigmented rats, zinc deficiency yielded an accumulation of lipofuscin in the RPE and of large pigmented macrophages in the choroids as well as the appearance of thin, rangy macrophages at Bruch's membrane. Moreover, we showed that a zinc diet reduced the zinc mole fraction of melanosomes in the RPE and modulated the thickness of the Bruch's membrane.
Highlights
Age-related macular degeneration (AMD), a disease that typically affects both eyes at different rates, is the leading cause of irreversible blindness among Caucasians over the age of 65 in the Western world [1,2,3]
Primary lesions associated with loss of vision in AMD are believed to be located in the retinal pigment epithelium (RPE) [5]
The quantification of lipofuscin granules was performed by electron microscopy; the fluorescent micrographs show clearly an increase of auto-fluorescent granules in the RPE from the ZD-Long Evans (LE) animals compared to the LE control rats (Figs. 2B and 2D)
Summary
Age-related macular degeneration (AMD), a disease that typically affects both eyes at different rates, is the leading cause of irreversible blindness among Caucasians over the age of 65 in the Western world [1,2,3]. The content of melanosomes in RPE cells decreases and melanosomes undergo age-related changes while the amount of lipofuscin and melanolipofuscin granules increases [6,7,8]. Age-related macular degeneration (AMD) is associated with lipofuscin accumulation whereas the content of melanosomes decreases. As the most affected group for AMD, is prone to zinc deficit, we investigated the chemical and ultrastructural effects of zinc deficiency in pigmented rat eyes after a six-month zinc penury diet
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