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Antioxidants and Cardiovascular Disease

  • Jean-Claude Tardif
  • Martial G. Bourassa

Part of the Developments in Cardiovascular Medicine book series (DICM, volume 233)

Table of contents

  1. Front Matter
    Pages i-xii
  2. Richard Gallo, Valentin Fuster
    Pages 19-46
  3. Marc Forgione, Joseph Loscalzo
    Pages 47-56
  4. Aalt Bast, Guido R. M. M. Haenen
    Pages 71-83
  5. Paolo Rubba, Mario Mancini
    Pages 85-100
  6. John F. Keaney Jr.
    Pages 101-116
  7. Christian Binggeli, Isabella Sudano, Georg Noll, Thomas F. Lüscher
    Pages 117-134
  8. Antoine Lafont, François Vinchon, Faouzi Addad, Eric Durand
    Pages 161-174
  9. Jean-Claude Tardif, Jean Grégoire, Martial G. Bourassa
    Pages 175-191
  10. Douglas B. Sawyer, Wilson S. Colucci
    Pages 193-209
  11. Michel White, Jean-Claude Tardif, Martial G. Bourassa
    Pages 211-224
  12. Jawahar L. Mehta, Dayuan Li, Jason Mehta
    Pages 225-238
  13. Back Matter
    Pages 239-258

About this book

Introduction

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.

Keywords

Lipid Lipoprotein Oxidation Pathogene antioxidant cardiovascular cardiovascular disease cytokine heart intervention medicine metabolism prevention proteins vascular disease

Editors and affiliations

  • Jean-Claude Tardif
    • 1
  • Martial G. Bourassa
    • 1
  1. 1.Montreal Heart Institute, Research Center and Department of Medicine, Faculty of MedicineUniversity of MontrealMontrealCanada

Bibliographic information

  • DOI https://doi.org/10.1007/978-94-011-4375-2
  • Copyright Information Kluwer Academic Publishers 2000
  • Publisher Name Springer, Dordrecht
  • eBook Packages Springer Book Archive
  • Print ISBN 978-94-010-5881-0
  • Online ISBN 978-94-011-4375-2
  • Series Print ISSN 0166-9842
  • Buy this book on publisher's site
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