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      Production of Free Radicals and Oxygen Consumption by Primary Equine Endothelial Cells During Anoxia-Reoxygenation

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          Abstract

          The endothelium plays an active role in ischemia/reperfusion injuries. Herein, we report the effect of a single or successive cycles of anoxia/reoxygenation (A/R) on the mitochondrial respiratory function of equine endothelial cells (cultured from carotids) monitored by high resolution oxymetry, and on their production of reactive oxygen species (ROS). ROS were measured by electron paramagnetic resonance (ESR) using POBN and DMPO spin traps, and by gas chromatography (GC) of ethylene released by ROS-induced α-keto-γ-(methylthio)butyric acid (KMB) oxidation. The oxygen consumption significantly decreased with the number of A/R cycles, and POBN-ESR spectra were specific of adducts formed in the cells from superoxide anion. After a one-hour A/R cycle, high intensity DMPO-ESR spectra were observed and assigned to superoxide anion trapping; the GC results confirmed an important production of ROS compared to normoxic cells. These results show that A/R induces mitochondrial alterations in endothelial cells, and strongly stimulates their oxidative activity as demonstrated by ESR and GC methods.

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          Role of reactive oxygen species (ROS) in apoptosis induction.

          H U Simon, A. HAJ-YEHIA, F. Levi-Schaffer (2000)
          Reactive oxygen species (ROS) and mitochondria play an important role in apoptosis induction under both physiologic and pathologic conditions. Interestingly, mitochondria are both source and target of ROS. Cytochrome c release from mitochondria, that triggers caspase activation, appears to be largely mediated by direct or indirect ROS action. On the other hand, ROS have also anti-apoptotic effects. This review focuses on the role of ROS in the regulation of apoptosis, especially in inflammatory cells.
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            Endothelial dysfunction in diabetes.

            A De Vriese, T J Verbeuren, J. Van de Voorde … (2000)
            Endothelial dysfunction plays a key role in the pathogenesis of diabetic vascular disease. The endothelium controls the tone of the underlying vascular smooth muscle through the production of vasodilator mediators. The endothelium-derived relaxing factors (EDRF) comprise nitric oxide (NO), prostacyclin, and a still elusive endothelium-derived hyperpolarizing factor (EDHF). Impaired endothelium-dependent vasodilation has been demonstrated in various vascular beds of different animal models of diabetes and in humans with type 1 and 2 diabetes. Several mechanisms of endothelial dysfunction have been reported, including impaired signal transduction or substrate availibility, impaired release of EDRF, increased destruction of EDRF, enhanced release of endothelium-derived constricting factors and decreased sensitivity of the vascular smooth muscle to EDRF. The principal mediators of hyperglycaemia-induced endothelial dysfunction may be activation of protein kinase C, increased activity of the polyol pathway, non-enzymatic glycation and oxidative stress. Correction of these pathways, as well as administration of ACE inhibitors and folate, has been shown to improve endothelium-dependent vasodilation in diabetes. Since the mechanisms of endothelial dysfunction appear to differ according to the diabetic model and the vascular bed under study, it is important to select clinically relevant models for future research of endothelial dysfunction.
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              Mitochondria in health and disease: perspectives on a new mitochondrial biology.

              Michael Duchen (2004)
              The integrity of mitochondrial function is fundamental to cell life. It follows that disturbances of mitochondrial function will lead to disruption of cell function, expressed as disease or even death. In this review, I consider recent developments in our knowledge of basic aspects of mitochondrial biology as an essential step in developing our understanding of the contributions of mitochondria to disease. The identification of novel mechanisms that govern mitochondrial biogenesis and replication, and the delicately poised signalling pathways that coordinate the mitochondrial and nuclear genomes are discussed. As fluorescence imaging has made the study of mitochondrial function within cells accessible, the application of that technology to the exploration of mitochondrial bioenergetics is reviewed. Mitochondrial calcium uptake plays a major role in influencing cell signalling and in the regulation of mitochondrial function, while excessive mitochondrial calcium accumulation has been extensively implicated in disease. Mitochondria are major producers of free radical species, possibly also of nitric oxide, and are also major targets of oxidative damage. Mechanisms of mitochondrial radical generation, targets of oxidative injury and the potential role of uncoupling proteins as regulators of radical generation are discussed. The role of mitochondria in apoptotic and necrotic cell death is seminal and is briefly reviewed. This background leads to a discussion of ways in which these processes combine to cause illness in the neurodegenerative diseases and in cardiac reperfusion injury. The demands of mitochondria and their complex integration into cell biology extends far beyond the provision of ATP, prompting a radical change in our perception of mitochondria and placing these organelles centre stage in many aspects of cell biology and medicine.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Open Biochem J
                Journal ID (publisher-id): TOBIOCJ
                Title: The Open Biochemistry Journal
                Publisher: Bentham Open
                ISSN (Electronic): 1874-091X
                Publication date (Electronic): 24 November 2011
                Publication date Collection: 2011
                Volume: 5
                Pages: 52-59
                Affiliations
                [1 ]Department of Clinical Sciences, Equine Clinic, Faculty of Veterinary Medicine B41, University of Liège, Sart Tilman, 4000 Liège, Belgium
                [2 ]Center for Oxygen Research and Development, Institute of Chemistry B6a, University of Liège, Sart Tilman, 4000 Liège, Belgium
                Author notes
                [* ]Address correspondence to these authors at the Center for Oxygen Research and Development, Institute of Chemistry B6a, University of Liège, Sart Tilman, 4000 Liège, Belgium; Tel: +32 4-366-33-66; Fax: +32 4-366-28-66; E-mails: g.delarebieredepouyade@ 123456ulg.ac.be ; amouithys@ 123456ulg.ac.be
                Article
                Publisher ID: TOBIOCJ-5-52
                DOI: 10.2174/1874091X01105010052
                PMC ID: 3242399
                PubMed ID: 22207886
                SO-VID: b6d9ff70-e327-4062-97ba-3dc0d46a038b
                Copyright © © de la Rebière de Pouyade et al.; Licensee Bentham Open.
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 28 August 2011
                Date revision received : 1 October 2011
                Date accepted : 10 October 2011
                Categories
                Subject: Article

                ScienceOpen disciplines: Biochemistry
                Keywords: equine endothelial cell,reactive oxygen species,gas chromatography,high-resolution oxygraphy,electron spin resonance,anoxia/re-oxygenation,free radicals.
                Data availability:
                ScienceOpen disciplines: Biochemistry
                Keywords: equine endothelial cell, reactive oxygen species, gas chromatography, high-resolution oxygraphy, electron spin resonance, anoxia/re-oxygenation, free radicals.

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