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[Reduction of lipid peroxidation and apoptosis in corneal endothelial cells by vitamin A].

Augenklinik, SMZ-Ost des Donauspitals, Wien, Osterreich.
Der Ophthalmologe (Impact Factor: 0.72). 07/2005; 102(6):607-13.
Source: PubMed

ABSTRACT The goal of this study was to determine the effects of lipid peroxidation-mediated toxicity of iron ions on corneal endothelial cells leading to apoptosis.
Murine corneal endothelial cells were maintained in tissue culture medium supplemented with free iron ions, known to lead to increased lipid peroxidation. Retinoic acid in the cell supernatant and cytoplasm of these cells was determined using HPLC. The rate of apoptosis was assessed by quantification of caspase-3-like activity. The lipid peroxidation was measured using the malondialdehyde method. Supplementation of retinoic acid was tested in the setting of apoptosis.
Free iron ions led to a rapid loss of retinoic acid in the supernatant and the corneal endothelial cells. This was correlated with rising levels of malondialdehyde following oxidative stress and increased apoptosis. Supplementation of retinoic acid alone significantly reduced oxidative stress and apoptosis in the respective cells.
In this study the authors present a novel in vitro model to test the direct influence of pro-oxidative species on corneal endothelial cells. The authors also prove that supplementing corneal endothelial cells with retinoic acid sufficiently prevents free radical injury and apoptosis.

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    • "The concentration of vitamin E has been inversely correlated to LPO (Selvendiran and Sakthisekaran, 2004). Vitamin A as an antioxidant is involved in counteracting free radicals and is known to help in the repair of damaged tissues (Serbecic et al., 2005). Vitamin A at pharmacological doses is reported to ameliorate oxidative stress mediated membrane lipid peroxidation and membranes enriched with vitamin A are protected against oxidative stress in vivo and exhibit resistance to LPO induced in vitro (Britton et al., 2000). "
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    • "The concentration of vitamin E has been inversely correlated to LPO (Selvendiran and Sakthisekaran, 2004). Vitamin A as an antioxidant is involved in counteracting free radicals and is known to help in the repair of damaged tissues (Serbecic et al., 2005). Vitamin A at pharmacological doses is reported to ameliorate oxidative stress mediated membrane lipid peroxidation and membranes enriched with vitamin A are protected against oxidative stress in vivo and exhibit resistance to LPO induced in vitro (Britton et al., 2000). "
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