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S.M. Conley, Z. Wan, S. Coons, W. Stamer; Functional Alterations in the Trabecular Meshwork After Selenium Treatment . Invest. Ophthalmol. Vis. Sci. 2006;47(13):427.
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The Nutritional Prevention of Cancer intervention trial has reported an increased incidence of glaucoma in selenium–supplemented individuals. Previously, we have shown that selenium inhibits key measures of trabecular meshwork (TM) homeostasis including protein synthesis, protein secretion, and cell–cell adhesion. The purpose of the present study was to investigate the effects of selenium on two aspects of TM function.
Confluent human TM cells were pre–treated with 2 and 5 µM methylseleninic acid (selenium), and then incubated with fluorescently labeled, linearized DNA. After fixation, cells that phagocytosed labeled DNA were counted by two different methods: flow cytometry of trypsinized cells and fluorescence microscopy of stable monolayers. Anterior segments were dissected from human cadaver eyes according to established procedures, mounted into perfusion chambers and perfused in the presence or absence of selenium (5–10 µM) at a flow rate of 2.5 µl/min.
Selenium treatment decreased the phagocytic capacity of two TM cell lines by approximately 25% as measured by two distinct methods. After establishing a stable baseline, exposure of human anterior segments to selenium resulted in a 15–30% (s.d. 7%) decrease in outflow facility in perfused anterior segments (n=3). This decrease was observed by 48 hours after introduction of selenium and was reversible upon compound washout.
Results show that selenium, at physiologically relevant concentrations, inhibits two key measures of conventional outflow function. Alterations in the phagocytic activity of TM cells may lead to accumulation of debris in the meshwork and ultimately to a pathological increase in intraocular pressure.
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