The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Free radicals mediate endothelial cell dysfunction caused by elevated glucose
Abstract
Impaired endothelium-dependent relaxation occurs in diabetic rabbit aorta and normal aorta exposed to elevated concentrations of glucose and is prevented by cyclooxygenase inhibitors. The role of free radicals in the endothelial cell impairment was examined with free radical scavengers and in aortas from rabbits fed with probucol (1% wt/wt, a lipid-soluble antioxidant). Rings of aorta suspended for measurement of isometric tension were incubated for 6 h in control (5.5 mM) or elevated (44 mM) glucose. Impairment of endothelium-dependent relaxation to acetylcholine caused by exposure to elevated glucose was prevented by superoxide dismutase, catalase, deferoxamine, or allopurinol and did not occur in aortas from probucol-fed rabbits. Similarly, impairment of acetylcholine relaxations in aortas from alloxan-induced diabetic rabbits was restored to normal by superoxide dismutase. Oxygen-derived free radicals generated by xanthine oxidase also caused impaired acetylcholine relaxations. Exposure of aortic segments to elevated glucose or to xanthine oxidase caused a significant increase in release of immunoreactive prostanoids. These data indicate that the endothelial cell dysfunction caused by elevated glucose is mediated by free radicals that are likely generated through the increased cyclooxygenase catalysis occurring in the endothelium. Treatment with antioxidants protects against impaired endothelium-dependent relaxations caused by elevated glucose.
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Cites
Superoxide anion is involved in the breakdown of endothelium-derived vascular relaxing factor
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Erythrocyte Membrane Lipid Peroxidation and Glycosylated Hemoglobin in Diabetes
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Hunt, J. V., Smith, C. C. T., & Wolff, S. P. (1990) · Diabetes · doi:10.2337/diab.39.11.1420 · Cited by 578
PGH synthase and lipoxygenase generate superoxide in the presence of NADH or NADPH.
Kukreja, R. C., Kontos, H. A., Hess, M. L., & Ellis, E. F. (1986) · Circulation Research · doi:10.1161/01.res.59.6.612 · Cited by 487
Oxygen-derived free radicals, endothelium, and responsiveness of vascular smooth muscle
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Hyperglycemia Can Cause Membrane Lipid Peroxidation and Osmotic Fragility in Human Red Blood Cells
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Role of Oxidative Modifications in Atherosclerosis
Stocker, R., & Keaney, J. F. (2004) · Physiological Reviews · doi:10.1152/physrev.00047.2003 · Cited by 2,624
Shared Risk Factors in Cardiovascular Disease and Cancer
Koene, R. J., Prizment, A. E., Blaes, A., & Konety, S. H. (2016) · Circulation · doi:10.1161/circulationaha.115.020406 · Cited by 1,494
Ceriello, A., & Motz, E. (2004) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.0000122852.22604.78 · Cited by 1,378
Endothelial dysfunction in diabetes
De Vriese, A. S., Verbeuren, T. J., Van de Voorde, J., Lameire, N. H., & Vanhoutte, P. M. (2000) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0703393 · Cited by 1,165
Impaired nitric oxide-mediated vasodilation in patients with non-insulin-dependent diabetes mellitus
Williams, S. B., Cusco, J. A., Roddy, M.-A., Johnstone, M. T., & Creager, M. A. (1996) · Journal of the American College of Cardiology · doi:10.1016/0735-1097(95)00522-6 · Cited by 1,014
Metadata
- Authors
- Tesfamariam, B., & Cohen, R. A.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 1992-08-01
- Volume
- 263
- Issue
- 2
- Pages
- H321-H326
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W1834350010
- Cited by
- 552
- References
- 19
- FWCI
- 8.53
- Type
- journal article
- Language
- en
- Open access
- closed
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- Tesfamariam, B., & Cohen, R. A. (1992). Free radicals mediate endothelial cell dysfunction caused by elevated glucose. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.1992.263.2.h321
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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