Abstract
Purpose: :
Age-related macular degeneration (AMD), the leading cause of blindness in western world, is associated with lipofuscin accumulation whereas the melanosome content declines. Melanosomes are the main storage of zinc in the pigmented tissues. Since the elderly population, 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.
Methods: :
Adult Long Evans (LE) rats were kept in zinc deficiency nutrition for six months. The control animals were fed with normal alimentation. Light, fluorescence and electron microscopy, as well as immunohistochemistry were performed. The number of photoreceptor nuclei, the number of lipofuscin granules as well as immunohistochemistry of cells found in the choroid of zinc deficiency (ZD) pigmented rats were quantified. Quantitative EDX analysis yielded the zinc mole fraction of melanosomes.
Results: :
The number of photoreceptor nuclei of zinc deficiency rats (ZD-LE) was significantly decreased and the number of the lipofuscin granules was found to be significantly increased in ZD-LE when compared to control rats. Moreover, ED1-positive cells were detected in the choroid of ZD-LE animals. EDX analysis showed that control melanosomes of the retinal pigment epithelium (RPE) of untreated rats contained 0.06 +/-0.02 at% zinc, while melanosomes of zinc deficient RPE showed no detectable zinc (0.01+/-0.01 at%). In contrast, the chemical composition of choroidal melanosomes did not change with respect to controls.
Conclusions: :
In pigmented animals, the zinc deficiency yields an accumulation of lipofuscin, pigmented macrophages in their choroids and a degeneration of photoreceptors. Moreover, we showed that zinc deficiency reduces the mole fraction of zinc in melanosomes of the RPE.
Keywords: ipofuscin • age-related macular degeneration • retinal pigment epithelium