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      Electron paramagnetic resonance spectroscopy in radiation research: Current status and perspectives

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          Abstract

          Exposure to radiation leads to a number of health-related malfunctions. Ionizing radiation is more harmful than non-ionizing radiation, as it causes both direct and indirect effects. Irradiation with ionizing radiation results in free radical-induced oxidative stress. Free radical-mediated oxidative stress has been implicated in a plethora of diseased states, including cancer, arthritis, aging, Parkinson's disease, and so on. Electron Paramagnetic Resonance (EPR) spectroscopy has various applications to measure free radicals, in radiation research. Free radicals disintegrate immediately in aqueous environment. Free radicals can be detected indirectly by the EPR spin trapping technique in which these forms stabilize the radical adduct and produce characteristic EPR spectra for specific radicals. Ionizing radiation-induced free radicals in calcified tissues, for example, teeth, bone, and fingernail, can be detected directly by EPR spectroscopy, due to their extended stability. Various applications of EPR in radiation research studies are discussed in this review.

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          Free radicals in the physiological control of cell function.

          Wulf Dröge (2002)
          At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, however, nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and reestablish "redox homeostasis." Higher organisms, however, have evolved the use of NO and ROS also as signaling molecules for other physiological functions. These include regulation of vascular tone, monitoring of oxygen tension in the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. NO and ROS are typically generated in these cases by tightly regulated enzymes such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. In a given signaling protein, oxidative attack induces either a loss of function, a gain of function, or a switch to a different function. Excessive amounts of ROS may arise either from excessive stimulation of NAD(P)H oxidases or from less well-regulated sources such as the mitochondrial electron-transport chain. In mitochondria, ROS are generated as undesirable side products of the oxidative energy metabolism. An excessive and/or sustained increase in ROS production has been implicated in the pathogenesis of cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and other diseases. In addition, free radicals have been implicated in the mechanism of senescence. That the process of aging may result, at least in part, from radical-mediated oxidative damage was proposed more than 40 years ago by Harman (J Gerontol 11: 298-300, 1956). There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.
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            Protein oxidation in aging, disease, and oxidative stress.

            Barbara S Berlett, E Stadtman (1997)
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              Free Radicals in Biology: Oxidative Stress and the Effects of Ionizing Radiation

              P.A. Riley (2009)
              The most important electron acceptor in the biosphere is molecular oxygen which, by virtue of its bi-radical nature, readily accepts unpaired electrons to give rise to a series of partially reduced species collectively known as reduced (or 'reactive') oxygen species (ROS). These include superoxide (O.2-), hydrogen peroxide (H2O2), hydroxyl radical (HO.) and peroxyl (ROO.) and alkoxyl (RO.) radicals which may be involved in the initiation and propagation of free radical chain reactions and which are potentially highly damaging to cells. Mechanisms have evolved to restrict and control such processes, partly by compartmentation, and partly by antioxidant defences such as chain-breaking antioxidant compounds capable forming stable free radicals (e.g. ascorbate, alpha-tocopherol) and the evolution of enzyme systems (e.g. superoxide dismutase, catalase, peroxidases) that diminish the intracellular concentration of the ROS. Although some ROS perform useful functions, the production of ROS exceeding the ability of the organism to mount an antioxidant defence results in oxidative stress and the ensuing tissue damage may be involved in certain disease processes. Evidence that ROS are involved in primary pathological mechanisms is a feature mainly of extraneous physical or chemical perturbations of which radiation is perhaps the major contributor. One of the important radiation-induced free-radical species is the hydroxyl radical which indiscriminately attacks neighbouring molecules often at near diffusion-controlled rates. Hydroxyl radicals are generated by ionizing radiation either directly by oxidation of water, or indirectly by the formation of secondary partially ROS. These may be subsequently converted to hydroxyl radicals by further reduction ('activation') by metabolic processes in the cell. Secondary radiation injury is therefore influenced by the cellular antioxidant status and the amount and availability of activating mechanisms. The biological response to radiation may be modulated by alterations in factors affecting these secondary mechanisms of cellular injury.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Pharm Bioallied Sci
                Journal ID (publisher-id): JPBS
                Title: Journal of Pharmacy and Bioallied Sciences
                Publisher: Medknow Publications Pvt Ltd (India )
                ISSN (Print): 0976-4879
                ISSN (Electronic): 0975-7406
                Publication date (Print): Apr-Jun 2010
                Volume: 2
                Issue: 2
                Pages: 80-87
                Affiliations
                [1]Division of CBRN Defence, Institute of Nuclear Medicine and Allied Sciences, Brig. S. K. Mazumdar Marg, Timarpur Delhi – 110054, India
                [1 ]Division of Chemistry and Biochemistry, Medical Faculty, Armeiska Street No. 11, Trakia University, Stara Zagora, Bulgaria
                [2 ]Department of Medical Elementology and Toxicology, Jamia Hamdard, Hamdard Nagar, New Delhi -110 062, India
                Author notes
                Address for correspondence: Dr. Rakesh Kumar Sharma, E-mail: rks@ 123456inmas.drdo.in
                Article
                Publisher ID: JPBS-2-80
                DOI: 10.4103/0975-7406.67006
                PMC ID: 3147108
                PubMed ID: 21814437
                SO-VID: de5bb9d8-975d-4cbf-bcd5-bff73d4fb500
                Copyright © © Journal of Pharmacy and Bioallied Sciences
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 08 April 2010
                Date revision received : 29 April 2010
                Date accepted : 21 May 2010
                Categories
                Subject: Invited Review

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: free radicals,ionizing radiation,radiation research,spin-trapping,oximetry,epr spectroscopy
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: free radicals, ionizing radiation, radiation research, spin-trapping, oximetry, epr spectroscopy

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