The ability of selenium to protect cultured human coronary artery endothelial cells (HCAEC), human umbilical vein endothelial cells (HUVEC) and bovine aortic endothelial cells (BAEC) from oxidative damage induced by 100 μM t-butyl hydroperoxide (t-BuOOH) was compared. Preincubation of human endothelial cells for 24 h with sodium selenite at concentrations as low as 5 nM provided significant protection against the harmful effects of 100 μM t-BuOOH, with complete protection being achieved with 40 nM selenite. The preincubation period was required for selenite to exert this protective effect on endothelial cells. When compared with selenium-deficient cells, the activities of cytoplasmic glutathione peroxidase (GPX-1), phospholipid hydroperoxide glutathione peroxidase (GPX-4) and thioredoxin reductase (TR) were each induced approx. 3–4-fold by 40 nM selenite. HCAEC and HUVEC showed great similarity in their relative abilities to resist oxidative damage in the presence and absence of selenite, and the activities of TR and the GPXs were also similar in these cell types. BAEC were more susceptible to damage by 100 μM t-BuOOH than were human endothelial cells, and could not be protected completely by incubation with selenite at concentrations up to 160 nM. The activity of TR in human endothelial cells was approx. 25-fold greater than that in BAEC of a similar selenium status, but GPX-1 and GPX-4 activities were not significantly different between the human and bovine cells. These studies, although performed with a small number of cultures, show for the first time that selenium at low doses can provide significant protection of the human coronary artery endothelium against damage by oxidative stress. TR may be an important antioxidant selenoprotein in this regard, in addition to the GPXs. The data also suggest that HUVEC, but not BAEC, represent a suitable model system in which to study the effects of selenium on the endothelium of human coronary arteries.
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Research Article|
April 05 2001
Selenite protects human endothelial cells from oxidative damage and induces thioredoxin reductase
Sue MILLER;
Sue MILLER
*University Department of Clinical Biochemistry, The Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, Scotland, U.K.
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Simon W. WALKER;
Simon W. WALKER
*University Department of Clinical Biochemistry, The Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, Scotland, U.K.
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John R. ARTHUR;
John R. ARTHUR
†Rowett Research Institute, Bucksburn, Aberdeen AB21 9SB, Scotland, U.K.
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Fergus NICOL;
Fergus NICOL
†Rowett Research Institute, Bucksburn, Aberdeen AB21 9SB, Scotland, U.K.
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Karen PICKARD;
Karen PICKARD
*University Department of Clinical Biochemistry, The Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, Scotland, U.K.
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Michelle H. LEWIN;
Michelle H. LEWIN
*University Department of Clinical Biochemistry, The Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, Scotland, U.K.
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A. Forbes HOWIE;
A. Forbes HOWIE
*University Department of Clinical Biochemistry, The Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, Scotland, U.K.
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Geoffrey J. BECKETT
*University Department of Clinical Biochemistry, The Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, Scotland, U.K.
Correspondence: Dr G. J. Beckett (e-mail [email protected]).
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Publisher: Portland Press Ltd
Received:
November 10 2000
Revision Received:
January 08 2001
Accepted:
February 08 2001
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 2001
2001
Clin Sci (Lond) (2001) 100 (5): 543–550.
Article history
Received:
November 10 2000
Revision Received:
January 08 2001
Accepted:
February 08 2001
Citation
Sue MILLER, Simon W. WALKER, John R. ARTHUR, Fergus NICOL, Karen PICKARD, Michelle H. LEWIN, A. Forbes HOWIE, Geoffrey J. BECKETT; Selenite protects human endothelial cells from oxidative damage and induces thioredoxin reductase. Clin Sci (Lond) 1 May 2001; 100 (5): 543–550. doi: https://doi.org/10.1042/cs1000543
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