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      Clinical Relevance of Biomarkers of Oxidative Stress

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          Significance: Oxidative stress is considered to be an important component of various diseases. A vast number of methods have been developed and used in virtually all diseases to measure the extent and nature of oxidative stress, ranging from oxidation of DNA to proteins, lipids, and free amino acids. Recent Advances: An increased understanding of the biology behind diseases and redox biology has led to more specific and sensitive tools to measure oxidative stress markers, which are very diverse and sometimes very low in abundance. Critical Issues: The literature is very heterogeneous. It is often difficult to draw general conclusions on the significance of oxidative stress biomarkers, as only in a limited proportion of diseases have a range of different biomarkers been used, and different biomarkers have been used to study different diseases. In addition, biomarkers are often measured using nonspecific methods, while specific methodologies are often too sophisticated or laborious for routine clinical use. Future Directions: Several markers of oxidative stress still represent a viable biomarker opportunity for clinical use. However, positive findings with currently used biomarkers still need to be validated in larger sample sizes and compared with current clinical standards to establish them as clinical diagnostics. It is important to realize that oxidative stress is a nuanced phenomenon that is difficult to characterize, and one biomarker is not necessarily better than others. The vast diversity in oxidative stress between diseases and conditions has to be taken into account when selecting the most appropriate biomarker. Antioxid. Redox Signal. 23, 1144–1170.

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          Most cited references 172

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          Oxygen-derived free radicals in postischemic tissue injury.

          It is now clear that oxygen-derived free radicals play an important part in several models of experimentally induced reperfusion injury. Although there are certainly multiple components to clinical ischemic and reperfusion injury, it appears likely that free-radical production may make a major contribution at certain stages in the progression of the injury. The primary source of superoxide in reperfused reoxygenated tissues appears to be the enzyme xanthine oxidase, released during ischemia by a calcium-triggered proteolytic attack on xanthine dehydrogenase. Reperfused tissues are protected in a variety of laboratory models by scavengers of superoxide radicals or hydroxyl radicals or by allopurinol or other inhibitors of xanthine oxidase. Dysfunction induced by free radicals may thus be a major component of ischemic diseases of the heart, bowel, liver, kidney, and brain.
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            Determination of carbonyl content in oxidatively modified proteins.

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              Beyond cholesterol. Modifications of low-density lipoprotein that increase its atherogenicity.


                Author and article information

                Antioxid Redox Signal
                Antioxid. Redox Signal
                Antioxidants & Redox Signaling
                Mary Ann Liebert, Inc. (140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA )
                10 November 2015
                10 November 2015
                : 23
                : 14
                : 1144-1170
                [ 1 ]Faculty of Health, Medicine and Life Sciences, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University , Maastricht, the Netherlands.
                [ 2 ]University of Exeter Medical School , Exeter, United Kingdom.
                [ 3 ]LabOS, Rudjer Boskovic Institute , Zagreb, Croatia.
                [ 4 ]Department of Medicine, Vanderbilt University , Nashville, Tennessee.
                [ 5 ]Division of Clinical Pharmacology, Department of Pharmacology, Vanderbilt University , Nashville, Tennessee.
                [ 6 ]Vascular Biology Division, Victor Chang Cardiac Research Institute , Darlinghurst, New South Wales, Australia.
                [ 7 ]School of Medical Sciences, University of New South Wales , Sydney, New South Wales, Australia.
                [ 8 ]Faculty of Medical Sciences, Goce Delcev University , Stip, Macedonia.
                [ 9 ]Centro de Investigación Biomedica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) , ISCIII, Madrid, Spain.
                [ 10 ]Instituto de Investigaciones Biomedicas “Alberto Sols” UAM-CSIC , Madrid, Spain.
                [ 11 ]Instituto de Investigacion Sanitaria La Paz (IdiPaz) , Madrid, Spain.
                [ 12 ]Department of Biochemistry, Faculty of Medicine, Autonomous University of Madrid , Madrid, Spain.
                [ 13 ]Department of Molecular Toxicology, German Institute of Human Nutrition (DIfE) , Nuthetal, Germany.
                [ 14 ]Faculty of Health Science, University of Copenhagen , Copenhagen, Denmark.
                [ 15 ]Bispebjerg-Frederiksberg Hospital , Copenhagen, Denmark.
                [ 16 ]Brighton and Sussex Medical School , Brighton, United Kingdom.
                Author notes
                Address correspondence to: Prof. Pietro Ghezzi, Brighton & Sussex Medical School Falmer, Brighton, United Kingdom

                E-mail: p.ghezzi@
                © Jeroen Frijhoff et al. 2015; Published by Mary Ann Liebert, Inc.

                This Open Access article is distributed under the terms of the Creative Commons Attribution Noncommercial License ( which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

                Page count
                Figures: 10, Tables: 7, Equations: 8, References: 202, Pages: 27
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