Antioxidants and Cardiovascular Disease:
Generation of oxidants or reactive oxygen species is a natural process of human biology. Mitochondrial respiration, phagocytic activity and cyclooxygenase activation are all essential processes of life, which also generate oxidative species. In humans, chronic oxidative stress often coupled with def...
Gespeichert in:
| Weitere Verfasser: | , |
|---|---|
| Format: | Elektronisch E-Book |
| Sprache: | English |
| Veröffentlicht: |
Dordrecht
Springer Netherlands
2000
|
| Schriftenreihe: | Developments in Cardiovascular Medicine
233 |
| Schlagworte: | |
| Online-Zugang: | UBR01 Volltext |
| Zusammenfassung: | Generation of oxidants or reactive oxygen species is a natural process of human biology. Mitochondrial respiration, phagocytic activity and cyclooxygenase activation are all essential processes of life, which also generate oxidative species. In humans, chronic oxidative stress often coupled with deficiency of antioxidant defenses is associated with the aging process and can lead to the development of disorders such as cancer and arterial disease. Major cardiovascular conditions in which oxidative damage has been strongly implicated include atherosclerosis, myocardial ischemia and reperfusion, coronary restenosis and congestive heart failure. Compelling evidence points to oxidative stress as an important trigger in the complex chain of events leading to atherosclerosis. The expression of chemotactic factors and adhesion molecules is modified by oxidative stress. Exposure to superoxide ions activates the NF-kappa B regulatory complex and triggers the transcription of several atherosclerosis related genes. These events lead to the accumulation of macrophages in the arterial wall. Macrophages avidly incorporate oxidized low-density lipoproteins (LDL) to form foam cells. The activity of matrix metalloproteinases is also regulated by oxidative stress. This activity appears to be closely coupled with smooth muscle cell activation and migration. Matrix metalloproteinases have also been implicated in the pathophysiology of plaque rupture. Antioxidant supplementation including vitamin E decreases susceptibility ofLDL to oxidation and retards the progression of atherosclerosis in animal models |
| Beschreibung: | 1 Online-Ressource (XII, 258 p) |
| ISBN: | 9789401143752 |
| DOI: | 10.1007/978-94-011-4375-2 |
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| 520 | |a Generation of oxidants or reactive oxygen species is a natural process of human biology. Mitochondrial respiration, phagocytic activity and cyclooxygenase activation are all essential processes of life, which also generate oxidative species. In humans, chronic oxidative stress often coupled with deficiency of antioxidant defenses is associated with the aging process and can lead to the development of disorders such as cancer and arterial disease. Major cardiovascular conditions in which oxidative damage has been strongly implicated include atherosclerosis, myocardial ischemia and reperfusion, coronary restenosis and congestive heart failure. Compelling evidence points to oxidative stress as an important trigger in the complex chain of events leading to atherosclerosis. The expression of chemotactic factors and adhesion molecules is modified by oxidative stress. Exposure to superoxide ions activates the NF-kappa B regulatory complex and triggers the transcription of several atherosclerosis related genes. These events lead to the accumulation of macrophages in the arterial wall. Macrophages avidly incorporate oxidized low-density lipoproteins (LDL) to form foam cells. The activity of matrix metalloproteinases is also regulated by oxidative stress. This activity appears to be closely coupled with smooth muscle cell activation and migration. Matrix metalloproteinases have also been implicated in the pathophysiology of plaque rupture. Antioxidant supplementation including vitamin E decreases susceptibility ofLDL to oxidation and retards the progression of atherosclerosis in animal models | ||
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Datensatz im Suchindex
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| discipline | Medizin |
| doi_str_mv | 10.1007/978-94-011-4375-2 |
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| indexdate | 2024-07-10T08:36:25Z |
| institution | BVB |
| isbn | 9789401143752 |
| language | English |
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| spelling | Antioxidants and Cardiovascular Disease edited by Jean-Claude Tardif, Martial G. Bourassa Dordrecht Springer Netherlands 2000 1 Online-Ressource (XII, 258 p) txt rdacontent c rdamedia cr rdacarrier Developments in Cardiovascular Medicine 233 Generation of oxidants or reactive oxygen species is a natural process of human biology. Mitochondrial respiration, phagocytic activity and cyclooxygenase activation are all essential processes of life, which also generate oxidative species. In humans, chronic oxidative stress often coupled with deficiency of antioxidant defenses is associated with the aging process and can lead to the development of disorders such as cancer and arterial disease. Major cardiovascular conditions in which oxidative damage has been strongly implicated include atherosclerosis, myocardial ischemia and reperfusion, coronary restenosis and congestive heart failure. Compelling evidence points to oxidative stress as an important trigger in the complex chain of events leading to atherosclerosis. The expression of chemotactic factors and adhesion molecules is modified by oxidative stress. Exposure to superoxide ions activates the NF-kappa B regulatory complex and triggers the transcription of several atherosclerosis related genes. These events lead to the accumulation of macrophages in the arterial wall. Macrophages avidly incorporate oxidized low-density lipoproteins (LDL) to form foam cells. The activity of matrix metalloproteinases is also regulated by oxidative stress. This activity appears to be closely coupled with smooth muscle cell activation and migration. Matrix metalloproteinases have also been implicated in the pathophysiology of plaque rupture. Antioxidant supplementation including vitamin E decreases susceptibility ofLDL to oxidation and retards the progression of atherosclerosis in animal models Cardiology Biochemistry, general Nutrition Epidemiology Biochemistry Antioxidans (DE-588)4142729-4 gnd rswk-swf Kardiovaskuläre Krankheit (DE-588)4024666-8 gnd rswk-swf Kardiovaskuläre Krankheit (DE-588)4024666-8 s Antioxidans (DE-588)4142729-4 s DE-604 Tardif, Jean-Claude edt Bourassa, Martial G. edt Erscheint auch als Druck-Ausgabe 9780792365648 Erscheint auch als Druck-Ausgabe 9789401143769 Erscheint auch als Druck-Ausgabe 9789401058810 https://doi.org/10.1007/978-94-011-4375-2 Verlag URL des Erstveröffentlichers Volltext |
| spellingShingle | Antioxidants and Cardiovascular Disease Cardiology Biochemistry, general Nutrition Epidemiology Biochemistry Antioxidans (DE-588)4142729-4 gnd Kardiovaskuläre Krankheit (DE-588)4024666-8 gnd |
| subject_GND | (DE-588)4142729-4 (DE-588)4024666-8 |
| title | Antioxidants and Cardiovascular Disease |
| title_auth | Antioxidants and Cardiovascular Disease |
| title_exact_search | Antioxidants and Cardiovascular Disease |
| title_full | Antioxidants and Cardiovascular Disease edited by Jean-Claude Tardif, Martial G. Bourassa |
| title_fullStr | Antioxidants and Cardiovascular Disease edited by Jean-Claude Tardif, Martial G. Bourassa |
| title_full_unstemmed | Antioxidants and Cardiovascular Disease edited by Jean-Claude Tardif, Martial G. Bourassa |
| title_short | Antioxidants and Cardiovascular Disease |
| title_sort | antioxidants and cardiovascular disease |
| topic | Cardiology Biochemistry, general Nutrition Epidemiology Biochemistry Antioxidans (DE-588)4142729-4 gnd Kardiovaskuläre Krankheit (DE-588)4024666-8 gnd |
| topic_facet | Cardiology Biochemistry, general Nutrition Epidemiology Biochemistry Antioxidans Kardiovaskuläre Krankheit |
| url | https://doi.org/10.1007/978-94-011-4375-2 |
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