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M. Zhang, T. Xiaio, L. Vergara, N. Ansari; Modification of Cytoskeletal Proteins by Lipid–Derived Aldehydes in the Lens Epithelial Cells . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2892.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: We have demonstrated earlier that 4–hydroxynonenal (HNE), a reactive lipid derived aldehyde is cataractogenic . It has been shown to modify the neuronal microtubules and cytoskeleton of fibroblasts and cardiomyocytes . Because disrupted lens cytoskeleton in the animal models of cataract and human cataract have been observed, we investigated if HNE mediates the disruption of lens cytoskeleton under conditions of oxidative stress. Methods: Human lens epithelial cell line (HLEC) and rat lenses were exposed to HNE or oxidants such as Fenton reagents and 50 mM glucose. In some experiments butylated hydroxytoluene (BHT) was added to ameliorate the oxidative stress. Apoptosis of HLEC was measured by the cell death detection ELISA kit and the opacity of the rat lens was measured using the image system. Immunohistochemistry and Western blots of HLEC and rat lens epithelia were performed using cytoskeletal antibodies such as anti–tubulin, anti–actin and anti–vimentin. Results: HNE induced apoptosis in HLEC starting as early as 1 hr of exposure as compared to 4 hrs by Fenton reagents. Both, HNE and Fenton reagents produced opacification in the rat lens at 72–96 hrs of incubation. Immunohistochemical studies and Western blots demonstrated a disruption in the cytoskeleton as well as loss of cytoskeletal proteins. Conclusions: Under oxidative stress, modification of the cytoskeletal proteins by HNE could be an important event resulting in apoptosis of the lens epithelial cells and lens opacification. Scavenging the oxidants and detoxification of HNE , in combination, may be an efficient preventive approach against oxidation–induced cataractogenesis.
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