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      Non-bulky Lesions in Human DNA: the Ways of Formation, Repair, and Replication

      research-article
      Author(s): , ,
      Publication date (Print):
      Journal: Acta Naturae
      Publisher: A.I. Gordeyev
      Keywords: DNA damage, DNA repair, DNA translesion synthesis

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          Abstract

          DNA damage is a major cause of replication interruption, mutations, and cell death. DNA damage is removed by several types of repair processes. The involvement of specialized DNA polymerases in replication provides an important mechanism that helps tolerate persistent DNA damage. Specialized DNA polymerases incorporate nucleotides opposite lesions with high efficiency but demonstrate low accuracy of DNA synthesis. In this review, we summarize the types and mechanisms of formation and repair of non-bulky DNA lesions, and we provide an overview of the role of specialized DNA polymerases in translesion DNA synthesis.

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          DNA base damage by reactive oxygen species, oxidizing agents, and UV radiation.

          Jean Scotty Cadet, J Wagner (2013)
          Emphasis has been placed in this article dedicated to DNA damage on recent aspects of the formation and measurement of oxidatively generated damage in cellular DNA in order to provide a comprehensive and updated survey. This includes single pyrimidine and purine base lesions, intrastrand cross-links, purine 5',8-cyclonucleosides, DNA-protein adducts and interstrand cross-links formed by the reactions of either the nucleobases or the 2-deoxyribose moiety with the hydroxyl radical, one-electron oxidants, singlet oxygen, and hypochlorous acid. In addition, recent information concerning the mechanisms of formation, individual measurement, and repair-rate assessment of bipyrimidine photoproducts in isolated cells and human skin upon exposure to UVB radiation, UVA photons, or solar simulated light is critically reviewed.
          Article 0 comments Cited 238 times – based on 0 reviews     Review now
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            Mitochondrial DNA damage is more extensive and persists longer than nuclear DNA damage in human cells following oxidative stress.

            F. M. Yakes, B. Van Houten (1997)
            A significant amount of reactive oxygen species (ROS) is generated during mitochondrial oxidative phosphorylation. Several studies have suggested that mtDNA may accumulate more oxidative DNA damage relative to nuclear DNA. This study used quantitative PCR to examine the formation and repair of hydrogen peroxide-induced DNA damage in a 16.2-kb mitochondrial fragment and a 17.7-kb fragment flanking the beta-globin gene. Simian virus 40-transformed fibroblasts treated with 200 microM hydrogen peroxide for 15 or 60 min exhibited 3-fold more damage to the mitochondrial genome compared with the nuclear fragment. Following a 60-min treatment, damage to the nuclear fragment was completely repaired within 1.5 hr, whereas no DNA repair in the mitochondrion was observed. Mitochondrial function, as assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide reduction, also showed a sharp decline. These cells displayed arrested-cell growth, large increases in p21 protein levels, and morphological changes consistent with apoptosis. In contrast, when hydrogen peroxide treatments were limited to 15 min, mtDNA damage was repaired with similar kinetics as the nuclear fragment, mitochondrial function was restored, and cells resumed division within 12 hr. These results indicate that mtDNA is a critical cellular target for ROS. A model is presented in which chronic ROS exposure, found in several degenerative diseases associated with aging, leads to decreased mitochondrial function, increased mitochondrial-generated ROS, and persistent mitochondrial DNA damage. Thus persistent mitochondrial DNA damage may serve as a useful biomarker for ROS-associated diseases.
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              DNA-damaging agents in cancer chemotherapy: serendipity and chemical biology.

              Kahlin Cheung-Ong, Guri Giaever, Corey Nislow (2013)
              DNA-damaging agents have a long history of use in cancer chemotherapy. The full extent of their cellular mechanisms, which is essential to balance efficacy and toxicity, is often unclear. In addition, the use of many anticancer drugs is limited by dose-limiting toxicities as well as the development of drug resistance. Novel anticancer compounds are continually being developed in the hopes of addressing these limitations; however, it is essential to be able to evaluate these compounds for their mechanisms of action. This review covers the current DNA-damaging agents used in the clinic, discusses their limitations, and describes the use of chemical genomics to uncover new information about the DNA damage response network and to evaluate novel DNA-damaging compounds. Copyright © 2013 Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                A.V. Makarova
                Journal
                Journal ID (nlm-ta): Acta Naturae
                Journal ID (iso-abbrev): Acta Naturae
                Journal ID (publisher-id): ActaNaturae
                Title: Acta Naturae
                Publisher: A.I. Gordeyev
                ISSN (Print): 2075-8251
                Publication date (Print): Jul-Sep 2017
                Volume: 9
                Issue: 3
                Pages: 12-26
                Affiliations
                Institute of Molecular Genetics of Russian Academy of Sciences, Kurchatov sq. 2, Moscow, 123182 , Russia
                Department of Molecular Biology, Faculty of Biology, Moscow State University, Leninskie Gory 1, bldg. 12, Moscow, 119991, Russia
                Article
                DOI: 10.32607/20758251-2017-9-3-12-26
                PMC ID: 5662270
                SO-VID: f5604385-c823-4bf5-90fb-d93412c5a61c
                Copyright © Copyright ® 2017 Park-media Ltd.
                License:

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

                History
                Date received : 29 May 2017
                Categories
                Subject: Research Article
                Subject: Molecular Biology

                ScienceOpen disciplines: Life sciences
                Keywords: dna damage,dna repair,dna translesion synthesis
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: dna damage, dna repair, dna translesion synthesis

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