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Effects Of Dexamethasone In The Lens

Conference paper
Authors Anne Petersen
Madeleine Zetterberg
Therese Carlsson
Johan Sjöstrand
Jan-Olof Karlsson
Published in Invest. Ophthalmol. Vis. Sci.
Volume 47
Issue 5
Pages 4110-
Publication year 2006
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 4110-
Language en
Subject categories Cell and Molecular Biology


Purpose: The aim of the study was to investigate effects of glucocorticoids in the lens. Methods: Lens epithelial cells (HLEC) were exposed to dexamethasone for 24 hours. Cells were assayed for changes in superoxide production using dihydroethidium (HET), for alterations in peroxide production using DCFH-DA or for GSH variations using monochlorobimane (MCB). Apoptosis was determined by Caspase-3 assay and by nuclear morphology of Hoechst stained cells. Mitochondria depolarisation was measured using the potential-sensitive colour JC-1. Morphology was examined by transmission electron microscopy (TEM). Results: Apoptosis were increased in HLEC exposed to 1, 10, 100 and 1000 {micro}M dexamethasone as revealed by nuclear morphology studies. Caspase-3 activity was increased at 100 and 1000 {micro}M dexamethasone. No effect on GSH, superoxide or peroxide production by dexamethasone was present. High concentrations of dexamethasone (1000 {micro}M) depolarised the mitochondria. TEM showed multilayering of cells, mitochondrial changes and accumulation of membrane delimited electron dense material. Conclusions: The mechanism underlying dexamethasone induced apoptosis and morphological changes in HLEC are probably not due to oxidative effects.

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