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D. Kokkinou, T. Schwarz, K. Bartz–Schmidt, U. Schraermeyer; Zinc Deficiency Leads to Lipofuscin Accumulation in Rats . Invest. Ophthalmol. Vis. Sci. 2005;46(13):256.
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Purpose: Age–related macular degeneration (AMD) is more prevalent among elderly Caucasians than Africans. Cross–linked high molecular weight proteins accumulating in Bruch’s membrane/choroid with age, are more pronounced in Caucasian than in African Americans. Zinc functions as an antioxidant, is important for physiological ocular operation and binds to melanin in pigmented tissues. The purpose of this study was to examine the role of melanin in the ocular tissues, using Long Evans (LE) and Wistar rats, in a zinc deficiency status. Methods: L.E and Wistar rats were kept for over 6 months on a zinc–free diet (5 animals per group). The same quantity was used as a control. The animals were clinically examined by electroretinography (ERG). The retina and choroid of the animals were further investigated using light, fluorescence and electron microscopy and histochemistry. Results: Zinc deficiency animals were more damaged compared to controls. Loss of photoreceptors was observed in both strains of zinc deficiency rats. However, the ERGs of the zinc–diet groups indicated a greater impairment of the pigmented animals compared to the Wistar rats. In addition, significant enhancement of lipofuscin accumulation, changes in shape and size of the melanosomes and infiltrating pigmented macrophages were detected only in the zinc deficiency L.E. rats. Conclusions: Our results indicated that melanin plays a crucial role in zinc metabolism. Zinc deficiency leads to lipofuscin accumulation in pigmented rats. The amount of ocular melanin and zinc decrease with age and elderly people are prone to a zinc deficiency status. In therapeutically trials of ocular diseases, e.g. AMD, the interaction of melanin and zinc should be taken into consideration.
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