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Cardiovascular Research 2000 47(3):410-418; doi:10.1016/S0008-6363(00)00097-3
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Lipid peroxidation, antioxidants and cardiovascular disease: how should we move forward?

Barry Halliwell

Department of Biochemistry, National University of Singapore, Kent Ridge Crescent, Singapore 119260, Singapore bchbh@nus.edu.sg

Received 27 January 2000; accepted 28 March 2000

KEYWORDS Coronary disease; Free radicals

The first 150 words of the full text of this article appear below.


    1 Introduction
 
It is widely agreed that increased consumption of fruits, grains and vegetables, decreased intake of saturated fats, a moderate degree of exercise and perhaps judicious consumption of red wine or other alcoholic beverages (or even tea) would improve the cardiovascular health of the populations in most developed and ‘near-developed’ countries [1–8]. Fruits, grains, teas, vegetables and red wines are rich in antioxidants (ascorbate, tocopherols, tocotrienols, flavonoids, other phenols and carotenoids are among the antioxidants found in various plants consumed by humans; reviewed in [9]), and so it is widely thought that antioxidants make an important contribution to this cardiovascular protective effect [9–14]. This assumption is logical, because there is good evidence that oxidative damage contributes to the pathology of atherosclerosis and vascular dysfunction generally, and that free radicals are involved in myocardial ischemia-reperfusion injury [9,15–20]. However, intervention trials with vitamin E that assess clinical end-points are . . . [Full Text of this Article]


    2 Are we asking the correct questions?
 

    3 Where are we now?
 

    4 Assaying lipid peroxidation
 
4.1 Direct assays of lipid peroxidation
4.2 Isoprostanes

    5 Conclusion
 

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