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The biological relevance of direct antioxidant effects of polyphenols for cardiovascular health in humans is not established
Journal of Nutrition, Volume 141, Issue 5, 1 May 2011, Pages 989S-1009S
Abstract
Human studies provide evidence for beneficial effects of polyphenol-rich foods on cardiovascular health. The antioxidant activity of polyphenols potentially explains these effects, but is the antioxidant activity a reliable predictor for these effects? An International Life Sciences Institute Europe working group addressed this question and explored the potential of antioxidant claims for polyphenols in relation to cardiovascular health by using the so-called Process for the Assessment of Scientific Support for Claims on Foods project criteria. In this process, analytical aspects of polyphenols, their occurrence in foods, dietary intake, and bioavailability were reviewed. Human studies on polyphenols and cardiovascular health were reviewed together with methods for biomarkers of oxidative damage and total antioxidant capacity (TAC). In retrospective studies, F2-isoprostanes and oxidized LDL, the most reliable biomarkers of lipid peroxidation, and measures for TAC showed the expected differences between cardiovascular disease patients and healthy controls, but prospective studies are lacking, and a causal relationship between these biomarkers and cardiovascular health could not be established. Therefore, the physiological relevance of a potential change in these biomarkers is unclear. We found limited evidence that some types of polyphenol-rich products modify these biomarkers in humans. A direct antioxidant effect of polyphenols in vivo is questionable, however, because concentrations in blood are low compared with other antioxidants and extensive metabolism following ingestion lowers their antioxidant activity. Therefore, the biological relevance of direct antioxidant effects of polyphenols for cardiovascular health could not be established. Overall, although some polyphenol-rich foods exert beneficial effects on some biomarkers of cardiovascular health, there is no evidence that this is caused by improvements in antioxidant function biomarkers (oxidative damage or antioxidant capacity). © 2011 American Society for Nutrition.
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Atherosclerosis
Volume 202, Issue 2, February 2009, Pages 321-329
doi:10.1016/j.atherosclerosis.2008.06.006 | How to Cite or Link Using DOI
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Review
The biological relevance and measurement of plasma markers of oxidative stress in diabetes and cardiovascular disease

This article is not included in your organization's subscription. However, you may be able toaccess this article under your organization's agreement with Elsevier.
Jeffrey W. Stephensa,b,,, Manish P. Khanolkara and Stephen C. Bainb
aDepartment of Diabetes & Endocrinology, Morriston Hospital, Swansea SA6 6NL, UK
bInstitute of Life Sciences, Swansea University, Swansea SA2 8PP, UK
Received 31 December 2007;
revised 14 May 2008;
accepted 11 June 2008.
Available online 20 June 2008.
Abstract
Oxidative stress is associated with many chronic diseases. In this review, we look at the role that oxidative stress may play in diabetes and related cardiovascular disease (CVD) and how oxidative damage may be measured in the plasma. Increased production of reactive oxygen species (ROS) has been implicated in the initiation and progression of both of these conditions and it may be that oxidative stress accounts for the unexplained increase in cardiovascular risk observed in diabetes. Plasma measurements are difficult because of the highly reactive nature of these molecules. Several studies have focused on measuring the total antioxidant buffering capacity of plasma or alternatively specific measures of free radical-mediated damage such as F2-isoprostane or oxidised-LDL (Ox-LDL). Perhaps, in the future, the discovery of an ‘easy to measure marker’ of oxidative stress might be incorporated into risk prediction in diabetes and cardiovascular disease.
Keywords: Oxidative stress; Diabetes; Cardiovascular disease; Risk; Biomarker
Article Outline
1.Introduction
2.The biological relevance of oxidative stress
3.Oxidative stress and diabetes mellitus
4.Glucose independent sources of oxidative stress
5.Oxidative stress and coronary heart disease
6.Oxidation of LDL and coronary heart disease
7.Measuring oxidative stress in plasma
7.1.Measuring the net antioxidant capacity of plasma 7.2.Plasma F2-isoprostanes 7.3.Other specific measures of oxidative damage
8.Conclusion
Acknowledgements
References

Fig. 1. Causes and consequences of Oxidative stress. ROS: Reactive oxygen species; MMP: Matrix metalloproteinases; VSMC: Vascular smooth muscle cell.
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Fig. 2. Hyperglycaemia induced oxidative stress. AGEs: Advanced glycosylation end-products; O2−: Superoxide radical; NOO−: Peroxynitrite radical.
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Fig. 3. Glucose and fatty acid dependent generation of ROS in the mitochondria.
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Fig. 4. Glucose independent sources of ROS.
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Table 1. Consequences of elevated Ox-LDL
MCP-1: Monocyte chemotactic protein-1; IL-1: I nterleunkin-1; ICAMs: Intercellular adhesion molecules; SAA: Serum amyloid A; PPARγ: Peroxisome proliferator-activated receptor-gamma.
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Table 2. Methods used to measure oxidative stress in plasma
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Corresponding author at: Diabetes Research Group, Institute of Life Sciences, Swansea University, Swansea SA2 8PP, UK. Tel.: +44 1792 704078; fax: +44 1792 703214.
Copyright © 2008 Elsevier Ireland Ltd All rights reserved.
Atherosclerosis
Volume 202, Issue 2, February 2009, Pages 321-329


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