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1.	Petersen, Anne, 1962, et al. (author) Effects Of Dexamethasone In The Lens 2006 In: Invest. Ophthalmol. Vis. Sci.. ; 47:5, s. 4110- Conference paper (peer-reviewed)abstract 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.

Petersen, Anne, 1962, et al. (author)
Effects Of Dexamethasone In The Lens
2006
In: Invest. Ophthalmol. Vis. Sci.. ; 47:5, s. 4110-
Conference paper (peer-reviewed)abstract
- 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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