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M. Zhang, V. U. L. Mokkapati, T. Xiao, G. A. Campbell, N. H. Ansari; Amelioration of Oxidation-Induced Toxicity in Human Lens Epithelial Cells and Diabetic Rat Lens by EDTA. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2434.
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Increased generation of oxidants, an inadequate redox system, or both have been suggested to be the key trigger for the development of cataract. Transition metals have been implicated in the generation of free radicals and their associated pathologies, such as cataractogenesis. We have therefore evaluated the efficacy of the metal chelator, EDTA in the prevention of toxicity in human lens epithelial cells (HLE) and rat lens exposed to various oxidants as well as diabetic rat lens. Because, EDTA does not freely enter into the cells, we used methylsulfonyl methane (MSM) with it as the permeability enhancer.
For the in vitro studies, HLEC and rat lens were exposed to various oxidants in the absence or presence of EDTA + MSM. Various markers of oxidative stress and toxicity were measured. For the in vivo studies, EDTA + MSM eye drop was applied daily to the diabetic rat eye. Cataractogenesis was monitored using the ophthalmoscope. At various time points, markers of oxidative stress and toxicity were determined in the lens.
Oxidative stress-induced markers as well as toxicity markers, which had increased in HLEC and rat lens exposed to oxidants, significantly normalized by including EDTA + MSM in the incubation medium. In the in vivo experiments, application of EDTA + MSM onto the diabetic rat eye, significantly delayed the formation of cataract.
Our results demonstrate that metal-catalyzed oxidation conditions used in this study, display common toxic parameters in HLEC and rat lens epithelium and that EDTA+MSM ameliorate these toxic parameters. Furthermore, our results demonstrating that topical application of EDTA+MSM onto the rat eye delays cataractogenesis, shows chelation therapy using these components may have immense clinical significance . Our studies have overcome the hurdle of permeability barrier and not being able to use metal chelators to prevent cataractogenesis.
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