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α-Lipoic acid and ascorbate prevent LDL oxidation and oxidant stress in endothelial cells

α-Lipoic acid and ascorbate prevent LDL oxidation and oxidant stress in endothelial cells Both α-lipoic acid (LA) and ascorbic acid (vitamin C) have been shown to improve endothelial dysfunction, a precursor of atherosclerosis. Since oxidant stress can cause endothelial dysfunction, we tested the interaction and efficacy of these antioxidants in preventing oxidant damage to lipids due to both intra- and extracellular oxidant stresses in EA.hy926 endothelial cells. LA spared intracellular ascorbate in culture and in response to an intracellular oxidant stress induced by the redox cycling agent menadione. Extracellular oxidant stress generated by incubating cells for 2 h in with 0.2 mg/ml LDL and 5 μM Cu2+ caused a time-dependent increase of the lipid peroxidation product malondialdehyde in both cells and LDL, preceded by rapid disappearance of` α-tocopherol in LDL. α-Lipoic acid at concentrations of 40–80 μM blunted these effects. Similarly, intracellular ascorbate concentrations of 1–2 mM also prevented Cu2+-induced lipid peroxidation in LDL and cells. Cu2+-dependent oxidation of LDL in the presence of ascorbate-loaded cells decreased intracellular ascorbate by 20%, but this decrease was not reversed by LA. Both LA and ascorbate protect endothelial cells and LDL from either intra- or extracellular oxidant stress, but that LA does not spare ascorbate in oxidatively stressed cells. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular and Cellular Biochemistry Springer Journals

α-Lipoic acid and ascorbate prevent LDL oxidation and oxidant stress in endothelial cells

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References (36)

Publisher
Springer Journals
Copyright
Copyright © 2007 by Springer Science+Business Media, LLC.
Subject
Life Sciences; Cardiology; Oncology ; Medical Biochemistry; Biochemistry, general
ISSN
0300-8177
eISSN
1573-4919
DOI
10.1007/s11010-007-9650-z
pmid
18026819
Publisher site
See Article on Publisher Site

Abstract

Both α-lipoic acid (LA) and ascorbic acid (vitamin C) have been shown to improve endothelial dysfunction, a precursor of atherosclerosis. Since oxidant stress can cause endothelial dysfunction, we tested the interaction and efficacy of these antioxidants in preventing oxidant damage to lipids due to both intra- and extracellular oxidant stresses in EA.hy926 endothelial cells. LA spared intracellular ascorbate in culture and in response to an intracellular oxidant stress induced by the redox cycling agent menadione. Extracellular oxidant stress generated by incubating cells for 2 h in with 0.2 mg/ml LDL and 5 μM Cu2+ caused a time-dependent increase of the lipid peroxidation product malondialdehyde in both cells and LDL, preceded by rapid disappearance of` α-tocopherol in LDL. α-Lipoic acid at concentrations of 40–80 μM blunted these effects. Similarly, intracellular ascorbate concentrations of 1–2 mM also prevented Cu2+-induced lipid peroxidation in LDL and cells. Cu2+-dependent oxidation of LDL in the presence of ascorbate-loaded cells decreased intracellular ascorbate by 20%, but this decrease was not reversed by LA. Both LA and ascorbate protect endothelial cells and LDL from either intra- or extracellular oxidant stress, but that LA does not spare ascorbate in oxidatively stressed cells.

Journal

Molecular and Cellular BiochemistrySpringer Journals

Published: Nov 16, 2007

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