14
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Static magnetic fields modulate X-ray-induced DNA damage in human glioblastoma primary cells

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Although static magnetic fields (SMFs) are used extensively in the occupational and medical fields, few comprehensive studies have investigated their possible genotoxic effect and the findings are controversial. With the advent of magnetic resonance imaging-guided radiation therapy, the potential effects of SMFs on ionizing radiation (IR) have become increasingly important. In this study we focused on the genotoxic effect of 80 mT SMFs, both alone and in combination with (i.e. preceding or following) X-ray (XR) irradiation, on primary glioblastoma cells in culture. The cells were exposed to: (i) SMFs alone; (ii) XRs alone; (iii) XR, with SMFs applied during recovery; (iv) SMFs both before and after XR irradiation. XR-induced DNA damage was analyzed by Single Cell Gel Electrophoresis assay (comet assay) using statistical tools designed to assess the tail DNA (TD) and tail length (TL) as indicators of DNA fragmentation. Mitochondrial membrane potential, known to be affected by IR, was assessed using the JC-1 mitochondrial probe. Our results showed that exposure of cells to 5 Gy of XR irradiation alone led to extensive DNA damage, which was significantly reduced by post-irradiation exposure to SMFs. The XR-induced loss of mitochondrial membrane potential was to a large extent averted by exposure to SMFs. These data suggest that SMFs modulate DNA damage and/or damage repair, possibly through a mechanism that affects mitochondria.

          Related collections

          Most cited references40

          • Record: found
          • Abstract: found
          • Article: not found

          Base excision repair of oxidative DNA damage and association with cancer and aging.

          Aging has been associated with damage accumulation in the genome and with increased cancer incidence. Reactive oxygen species (ROS) are produced from endogenous sources, most notably the oxidative metabolism in the mitochondria, and from exogenous sources, such as ionizing radiation. ROS attack DNA readily, generating a variety of DNA lesions, such as oxidized bases and strand breaks. If not properly removed, DNA damage can be potentially devastating to normal cell physiology, leading to mutagenesis and/or cell death, especially in the case of cytotoxic lesions that block the progression of DNA/RNA polymerases. Damage-induced mutagenesis has been linked to various malignancies. The major mechanism that cells use to repair oxidative damage lesions, such as 8-hydroxyguanine, formamidopyrimidines, and 5-hydroxyuracil, is base excision repair (BER). The BER pathway in the nucleus is well elucidated. More recently, BER was shown to also exist in the mitochondria. Here, we review the association of BER of oxidative DNA damage with aging, cancer and other diseases.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Role of oxidatively induced DNA lesions in human pathogenesis.

            Genome stability is essential for maintaining cellular and organismal homeostasis, but it is subject to many threats. One ubiquitous threat is from a class of compounds known as reactive oxygen species (ROS), which can indiscriminately react with many cellular biomolecules including proteins, lipids, and DNA to produce a variety of oxidative lesions. These DNA oxidation products are a direct risk to genome stability, and of particular importance are oxidative clustered DNA lesions (OCDLs), defined as two or more oxidative lesions present within 10 bp of each other. ROS can be produced by exposure of cells to exogenous environmental agents including ionizing radiation, light, chemicals, and metals. In addition, they are produced by cellular metabolism including mitochondrial ATP generation. However, ROS also serve a variety of critical cellular functions and optimal ROS levels are maintained by multiple cellular antioxidant defenses. Oxidative DNA lesions can be efficiently repaired by base excision repair or nucleotide excision repair. If ROS levels increase beyond the capacity of its antioxidant defenses, the cell's DNA repair capacity can become overwhelmed, leading to the accumulation of oxidative DNA damage products including OCDLs, which are more difficult to repair than individual isolated DNA damage products. Here we focus on the induction and repair of OCDLs and other oxidatively induced DNA lesions. If unrepaired, these lesions can lead to the formation of mutations, DNA DSBs, and chromosome abnormalities. We discuss the roles of these lesions in human pathologies including aging and cancer, and in bystander effects. Published by Elsevier B.V.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Oxidative depolymerization of polysaccharides by reactive oxygen/nitrogen species.

              Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are constantly produced and are tightly regulated to maintain a redox balance (or homeostasis) together with antioxidants (e.g. superoxide dismutase and glutathione) under normal physiological circumstances. These ROS/RNS have been shown to be critical for various biological events including signal transduction, aging, apoptosis, and development. Despite the known beneficial effects, an overproduction of ROS/RNS in the cases of receptor-mediated stimulation and disease-induced oxidative stress can inflict severe tissue damage. In particular, these ROS/RNS are capable of degrading macromolecules including proteins, lipids and nucleic acids as well as polysaccharides, and presumably lead to their dysfunction. The purpose of this review is to highlight (1) chemical mechanisms related to cell-free and cell-based depolymerization of polysaccharides initiated by individual oxidative species; (2) the effect of ROS/RNS-mediated depolymerization on the successive cleavage of the glycosidic linkage of polysaccharides by glycoside hydrolases; and (3) the potential biological outcome of ROS/RNS-mediated depolymerization of polysaccharides.
                Bookmark

                Author and article information

                Journal
                J Radiat Res
                J. Radiat. Res
                jrr
                jrr
                Journal of Radiation Research
                Oxford University Press
                0449-3060
                1349-9157
                March 2014
                17 December 2013
                17 December 2013
                : 55
                : 2
                : 218-227
                Affiliations
                [1 ]Radiation Development and Application, UTAPRAD-DIM, ENEA, Via Enrico Fermi 45, Frascati, Rome 00044, Italy
                [2 ]Fondazione San Raffaele, SS Ceglie San Michele Km 1.2, Ceglie Messapica 72013, Italy
                [3 ]Radiation Biology and Human Health UTBIORAD, ENEA, Via Anguillarese 301, Casaccia, Rome 00123, Italy
                [4 ]Institute of Biochemistry, University of Urbino ‘Carlo Bo’, Via Saffi 2, Urbino 61029, Italy
                [5 ]Institute of Biomathematics, University of Urbino ‘Carlo Bo’, Via Saffi 2, Urbino 61029, Italy
                [6 ]UPMC Paris 06, UR4 Aging, Stress and Inflammation, 7 Quai Saint Bernard, Paris 75252, France
                Author notes
                [* ]Corresponding author. UTAPRAD-DIM, ENEA, via Enrico Fermi 45, 00044 Frascati (Rome), Italy. Tel: +39-06-9400-5299; Fax: +39-06-94005770; Email: laura.teodori@ 123456enea.it
                Article
                rrt107
                10.1093/jrr/rrt107
                3951070
                24345558
                ee43483e-cb0f-41f2-85ff-411706dce0fc
                © The Author 2013. Published by Oxford University Press on behalf of The Japan Radiation Research Society and Japanese Society for Therapeutic Radiology and Oncology.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 13 December 2012
                : 26 July 2013
                : 2 August 2013
                Page count
                Pages: 10
                Categories
                Biology

                Oncology & Radiotherapy
                static magnetic field,ionizing radiation,comet assay,dna fragmentation,mitochondrial membrane potential,glioblastoma

                Comments

                Comment on this article