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Tesi sul tema "Oxidative damage"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 25 luglio 2025

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1

Yang, Weidong. "Oxidative damage of endothelial cells." Thesis, University of Leicester, 1999. http://hdl.handle.net/2381/29603.

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This study sought to investigate the consequences of different degrees of oxidative stress on endothelial cells, using a cultured endothelial cell model; principally bovine aortic endothelial cells, subjected to oxidative stress. High concentrations of H2O2 or a superoxide generating system caused rapid endothelial cell death, as evidenced by increased membrane permeability, which could be partially protected by myoglobin. Extracellular H2O2 caused a rapid increase in intracellular peroxidation but was also eliminated by endothelial cells. However, the anti-oxidant capacity of the bovine endot

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2

Soman, Sony. "OXIDATIVE DAMAGE TO DNA IN ALZHEIMER'S DISEASE." UKnowledge, 2013. http://uknowledge.uky.edu/chemistry_etds/28.

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Previous studies from our laboratory and others show a significant increase in levels of both nuclear and mitochondrial DNA and RNA oxidation in vulnerable brain regions in the progression of Alzheimer’s disease (AD). Although total DNA oxidation is increased in AD it remains unclear whether oxidative damage is widespread throughout the genome or is concentrated to specific genes. To test the hypothesis that specific genes are more highly oxidized in the progression of AD, we propose to quantify the percent oxidative damage in genes coding for proteins shown to be altered in the progression of

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3

Farooq, Sabya. "Free radical induced oxidative DNA damage." Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/30749.

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Oxidative DNA damage has been implicated in processes such as carcinogenesis, mutagenesis, ageing and cell death. Reactive oxygen species (ROS) such as superoxide (O2), hydrogen peroxide (H2O 2) and hydroxyl radical (OH*) are produced in mammalian cells as a result of aerobic metabolism. However excess generation of these species by endogenous or exogenous sources can result in damage to DNA, producing a large number of sugar and base lesions. In order to understand the biological consequences of such free radical induced damage it is essential to characterise and quantitate this damage. This

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4

Furness, Lindsay Jayne. "Energetics, oxidative damage and ageing in birds." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25473.

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5

Jansson, Kristina. "Oxidative damage and the DNA glycosylase MutYH /." Göteborg : Department of Cell and Molecular Biology, University of Gothenburg, 2010. http://hdl.handle.net/2077/22092.

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6

Davies, John McCartan Caswell. "Oxidative damage in the colon and rectum." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493554.

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There is considerable supportive evidence to suggest that increased levels of DNA damage are associated with an increased risk of developing neoplastic lesions in the human colon and rectum. Within this thesis, several different topics related to DNA damage were explored in detail, principally using the single cell gel electrophoresis assay (the comet assay) to measure DNA damage both in cell line studies and in human colorectal mucosal biopsies from patients undergoing routine endoscopic examinations of the colon and rectum.

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7

Konz, John O. (John Otto) 1971. "Oxidative damage to recombinant proteins during production." Thesis, Massachusetts Institute of Technology, 1998. http://hdl.handle.net/1721.1/17472.

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Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Chemical Engineering, 1998.<br>Includes bibliographical references (p. 209-222).<br>Since the introduction of recombinant human insulin nearly two decades ago, recombinant proteins have increasingly been utilized as therapeutic agents. In addition, expression of recombinant proteins is now a common tool used in basic research. Recombinant proteins are subject to many subtle modifications that can affect their properties; among these modifications, oxidative damage is one of the most ubiquitous. Oxidative damage, however, is only

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8

Renganathan, Kutralanathan. "Oxidative Damage and Age Related Macular Degeneration." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1193002743.

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9

Carroll, Luke Dean. "Modulation of oxidative damage by selenium compounds." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14124.

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Myeloperoxidase (MPO) is the primary enzyme responsible for the production of strong oxidants by neutrophils in response to pathogens. One of the major oxidants produced is hypochlorous acid (HOCl), which can react with amine groups to form the secondary oxidants N-chloramines. These oxidants play a role in the destruction of pathogens, however they also have the potential to damage host cells, and have been implicated in numerous inflammatory diseases. This Thesis explores the potential for selenium containing compounds and enzymes to act as catalytic oxidant scavengers. Reaction rates betwe

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10

Cao, Huachuan. "Probe Oxidative Damage in DNA Charge Transfer Process." Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/6983.

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As a hydrophilic biopolymer, a DNA molecule is surrounded by water molecules in aqueous solution. The charge hopping mechanism indicates the competition between radical cation quenching by water molecules and migration along DNA partially determines the distance and efficiency of charge transport in DNA. Lipid can effectively bind DNA to induce hydrophobic environment around the DNA helix and reduce the water contact with bases in the DNA duplex. Therefore, the effect of water molecules on charge transport can be studied by comparison between nature DNA and DNA-lipid complexes. We synthesized

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11

Karihtala, P. (Peeter). "Oxidative damage and counteracting mechanisms in breast carcinoma." Doctoral thesis, University of Oulu, 2006. http://urn.fi/urn:isbn:9514279530.

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Abstract Breast cancer is the leading cause of death from cancer among Finnish women, but the ultimate causation of carcinogenesis still remains unclear. Reactive oxygen species (ROS) is a collective term for several types of reactive oxygen metabolites that are continuously generated in human cells mainly as by-products of aerobic respiration. ROS, including nitric oxide and its derivatives, play highly important roles in cell physiology. If ROS production exceeds the capacity of detoxification systems, principally antioxidant enzymes, oxidative stress is said to occur. This state is known to

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12

Davies, Stefan M. K., and n/a. "Oxidative damage to mitochondria on ageing in rats." University of Otago. Department of Biochemistry, 2007. http://adt.otago.ac.nz./public/adt-NZDU20070403.111245.

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Ageing is a complex phenomenon, characterised by progressive loss of function, decreasing resistance to age-associated pathologies and stress, and increasing rates of mortality. The Free Radical Theory of Ageing implicates reactive oxygen and nitrogen species (ROS/RNS) generation as being integral to the ageing process, subjecting the organism to oxidative stress. Oxidative damage to biomolecules is suggested to be causative in the formation of ageing-associated phenotypes, dysregulation and dysfunction. Mitochondria are responsible for the production of the majority of ROS/RNS through norma

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13

Hannon-Fletcher, Mary Philomena Anne. "Oxidative stress and biomolecule damage in human IDDM." Thesis, University of Ulster, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322420.

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14

Hemming, Joanna. "Oxidative damage to lung surfactant and lipid membranes." Thesis, Birkbeck (University of London), 2015. http://bbktheses.da.ulcc.ac.uk/117/.

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Lung surfactant is a mixed monolayer of lipids and proteins that reduce the surface tension at the air-lung interface to prevent alveolar collapse. Exposure of lung surfactant to ozone pollution has been linked to an increased risk of death due to respiratory diseases. This work aimed to determine the ozone damage caused to lung surfactant at the air-water interface. A range of analytical techniques showed that peptide mimics of surfactant protein B were rapidly oxidised by ozone but no cleavage of the peptides occurred. Neutron reflectivity revealed that the peptides remained at the air-water

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15

Abdallah, Suaad Audat. "Investigation of Oxidative DNA Damage from Ionizing Radiation." University of Toledo Health Science Campus / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=mco1349377002.

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16

Gillham, David J. "Aspects of chloroplast protection against photo-oxidative damage." Thesis, University of Bath, 1986. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.373393.

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17

Woodall, Alan Anthony. "Carotenoids and the protection of membranes against oxidative damage." Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240900.

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18

Rehman, Almas. "Factors affecting oxidative DNA damage in the human body." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251611.

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19

Cochemé, Helena Margaret. "Yeast as a model for investigating mitochondrial oxidative damage." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614040.

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20

Rajaraman, Gnana Oli [Verfasser], and Helga [Akademischer Betreuer] Stopper. "Oxidative stress : role in genomic damage and disease = Oxidativer Stress / Gnana Oli Rajaraman. Betreuer: Helga Stopper." Würzburg : Universitätsbibliothek der Universität Würzburg, 2012. http://d-nb.info/1024851885/34.

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21

Elliott, Nathan Andrew. "Prevention of Oxidative Damage by Yeast and Human OXR1: A Dissertation." eScholarship@UMMS, 2004. https://escholarship.umassmed.edu/gsbs_diss/96.

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22

Ndlebe, Thabisile S. "Oxidative Damage in DNA: an Exploration of Various DNA Structures." Diss., Available online, Georgia Institute of Technology, 2006, 2006. http://etd.gatech.edu/theses/available/etd-05112006-154326/.

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Thesis (Ph. D.)--Chemistry and Biochemistry, Georgia Institute of Technology, 2007.<br>Donald F. Doyle, Committee Member ; Bridgette Anne Barry, Committee Member ; Dr. Gary B. Schuster, Committee Chair ; Nicholas V. Hud, Committee Member ; Roger M. Wartell, Committee Member.

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23

Cannan, Wendy J. "Mechanisms and Dynamics of Oxidative DNA Damage Repair in Nucleosomes." ScholarWorks @ UVM, 2016. http://scholarworks.uvm.edu/graddis/628.

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DNA provides the blueprint for cell function and growth, as well as ensuring continuity from one cell generation to the next. In order to compact, protect, and regulate this vital information, DNA is packaged by histone proteins into nucleosomes, which are the fundamental subunits of chromatin. Reactive oxygen species, generated by both endogenous and exogenous agents, can react with DNA, altering base chemistry and generating DNA strand breaks. Left unrepaired, these oxidation products can result in mutations and/or cell death. The Base Excision Repair (BER) pathway exists to deal with damage

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24

Clement, Amy Marie. "The Antioxidant Defense Network: Synergistic Combinations to Prevent Oxidative Damage." BYU ScholarsArchive, 2008. https://scholarsarchive.byu.edu/etd/1549.

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One of the matchless ironies of the human body is its requirement for the highly reactive oxygen molecule, which has been clearly implicated in many diseases and the aging processes. Oxidants produced by metabolic processes damage cells by starting chemical chain reactions including oxidation of DNA and proteins as well as lipid peroxidation. Damage to DNA can cause mutations and lead to cancer if not reversed by DNA repair mechanisms. Damage to proteins causes enzyme inhibition, denaturation and protein degradation. Lipid peroxidation can cause cell lysis as well as creating mutagenic and car

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25

Hyland, Paul. "DNA damage and mutation during extended culture of T cell clones in vitro : cause or effect of finite life span?" Thesis, University of Ulster, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.232861.

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26

Kappler, Marion. "Response of THP-1 cells to oxidative damage induced by AAPH." Thesis, University of Canterbury. School of Biological Sciences, 2005. http://hdl.handle.net/10092/2459.

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Monocyte cells can be damaged when exposed to reactive oxidative species during inflammatory events within the body. This research project has examined in detail the cellular events associated with free radical damage induced death of monocyte cells, using the water soluble peroxyl radical generator 2, 2' -azobis(2-methylpropionamidine) dihydrochloride (AAPH) as a model of inflammation induced oxidative stress. The human monocyte-derived cell line THP-1 was incubated with 10mM AAPH in Earle's Balanced Salt Solution at 37°C for up to 24 hours. Protein hydroperoxide formation was observed to occ

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27

Sohi, Gurmeet Kaur. "Measuring apparent oxidative damage to mitochondrial DNA by HIV antiretroviral therapy." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42278.

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Background/objectives: HIV antiretroviral therapy, specifically nucleoside reverse transcriptase inhibitors (NRTIs) have been associated with mitochondrial DNA (mtDNA) alterations, possibly through mtDNA oxidative damage leading to mitochondrial dysfunction, which is associated with degenerative diseases and aging. A published assay exploits that oxidative damage can slow down/inhibit DNA polymerase progression, such that the PCR amplification of damaged mtDNA template yields less product compared to undamaged mtDNA. I sought to optimize this assay using in-house tools and to quantify apparent

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28

Stathis, Dimitrios [Verfasser]. "Oxidative DNA Damage: From Lesion Chemistry to Biological Implications / Dimitrios Stathis." München : Verlag Dr. Hut, 2012. http://d-nb.info/1025821440/34.

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29

Quinlan, Gregory John. "Oxidative damage to extracellular proteins and lipids during acute lung injury." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281713.

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30

Fatima, Tehseen Zeb. "Mismatch repair in T. brucei : roles in protection against oxidative damage." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4554/.

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Cells are continuously exposed to different intracellular and extracellular mutagens, which can damage several different molecules, including DNA. To ensure survival, cells have evolved various defence and repair mechanisms. Mismatch repair (MMR) is the mechanism that serves to repair mismatched bases in DNA that are missed by the proof reading activity of DNA polymerases. Besides this, MMR also corrects base mismatches formed by altered bases modified by certain chemical mutagens. Thus, MMR is important to avoid mutagenesis and maintain genome fidelity. MMR is a complex, highly conserved path

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31

Allen, William Joseph. "Practical Applications of Molecular Modeling Pertaining to Oxidative Damage and Disease." Diss., Virginia Tech, 2011. http://hdl.handle.net/10919/78000.

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Molecular modeling is a term referring to the study of proteins, nucleic acids, lipids, and other bio- or macro- or small molecules at the atomistic level using a combination of computational methods, physico-chemical principles, and mathematical functions. It can be generally sub-divided into two areas: molecular mechanics, which is the treatment of atoms and bonds as Newtonian particles and springs, and quantum mechanics, which models electronic behaviors using the Schrödinger equation and wavefunctions. Each technique is a powerful tool that, when used alone or in combination with wet lab e

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32

Bhatkhande, Prajakta S. "Small Molecule Biomarkers Resulting from Radiation and Oxidative Damage to DNA." University of Toledo / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1470222983.

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33

Ye, Wenjie Ball Louise M. "Oxidative damage to guanine in DNA caused by reactive oxygen species." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,2457.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.<br>Title from electronic title page (viewed Sep. 3, 2009). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Environmental Sciences and Engineering,Gillings School of Global Public Health." Discipline: Environmental Sciences and Engineering; Department/School: Public Health.

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34

Mikhed, Yuliya [Verfasser]. "The role of DNA damage in the pathogenesis of nitrate tolerance - nitrosative versus oxidative DNA damage / Yuliya Mikhed." Mainz : Universitätsbibliothek Mainz, 2015. http://d-nb.info/1080187529/34.

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35

Alabarse, Paulo Vinicius Gil. "Estresse oxidativo e envelhecimento no encéfalo de ratos machos reprodutores." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2011. http://hdl.handle.net/10183/30205.

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A reprodução é capaz de alterar muitos parâmetros relacionados à fisiologia, ao comportamento e à morfologia em vertebrados machos. Trabalhos apresentam relação entre reprodução ou envelhecimento com estresse oxidativo, não havendo trabalho relacionando estresse oxidativo, reprodução e envelhecimento simultaneamente em mamíferos. Para avaliar o estresse oxidativo no encéfalo de ratos machos decorrente da atividade reprodutiva e ao longo do envelhecimento (3, 6, 12 e 24 meses) comparado a animais sem atividade reprodutiva (n = 10 por grupo e por idade), avaliou-se a atividade de enzimas antioxi

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36

Bona, Silvia Regina. "Melatonina protege o fígado em um modelo experimental de cirrose." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2014. http://hdl.handle.net/10183/129635.

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Base teórica: As doenças hepáticas representam um grande problema de saúde pública, sendo responsáveis por um considerável número de atendimentos e internações hospitalares, com crescente índice de mortalidade. A melatonina (MLT), uma potente molécula antioxidante, tem-se mostrado benéfica em diversas situações patológicas, incluindo as hepáticas. Objetivo: O objetivo foi avaliar os efeitos da MLT na cirrose hepática induzida por CCl4 em ratos machos Wistar. Métodos: Utilizaram-se 20 ratos machos Wistar, (230-250g), divididos em 4 grupos: I: Controle (CO), II: CO+MLT, III: CCl4 e IV: CCl4+MLT.

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37

Shaik, Raziya. "Photochemical Generation of the C5' -Uridinyl and Pseudouridinylradical for the Study of Oxidative Damage in RNA." University of Toledo / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1384518841.

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38

Sadi, Gokhan. "Oxidative Damage And Regulation Of Antioxidant Enzymes In Streptozotocin Induced Diabetic Rats." Phd thesis, METU, 2009. http://etd.lib.metu.edu.tr/upload/2/12611222/index.pdf.

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Increased oxidative stress and impaired antioxidant defense mechanisms are believed to be the important factors contributing to the pathogenesis and progression of diabetes mellitus. The products of lipid peroxidation and protein oxidation reactions were all found to be elevated significantly (p&lt<br>0.05) in diabetic animals and supplementing the animals either individually or in combination, with two powerful antioxidants DL-&amp<br>#945<br>-lipoic acid (LA) and vitamin C (VC) brought this increment toward the control values. Considering Cu-Zn SOD, CAT and GST-Mu, there was a significant de

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39

Xu, Meng. "Oxidative DNA Damage Modulates Trinucleotide Repeat Instability Via DNA Base Excision Repair." FIU Digital Commons, 2014. http://digitalcommons.fiu.edu/etd/1576.

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Trinucleotide repeat (TNR) expansion is the cause of more than 40 types of human neurodegenerative diseases such as Huntington’s disease. Recent studies have linked TNR expansion with oxidative DNA damage and base excision repair (BER). In this research, we provided the first evidence that oxidative DNA damage can induce CAG repeat deletion/contraction via BER. We found that BER of an oxidized DNA base lesion, 8-oxoguanine in a CAG repeat tract, resulted in the formation of a CTG hairpin at the template strand. DNA polymerase β (pol b) then skipped over the hairpin creating a 5’-flap that was

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40

Struthers, Louise. "An investigation of DNA damage induced by oxidative stress in neuronal cells." Thesis, University of Leicester, 1998. http://hdl.handle.net/2381/29576.

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This project aimed to investigate the hypothesis that oxidative DNA damage has a role in neuronal dysfunction. Reactive oxygen species (ROS) are known to damage important cellular macromolecules, including DNA. They have been implicated in many pathological conditions, including common neurodegenerative disorders, but the mechanisms of cellular dysfunction and death involved remain unclear. Oxidative DNA damage was therefore studied in an in vitro model system and pathological tissue. A novel, sensitive assay based on the fortuitous finding that avidin binds directly to the DNA lesion 8-oxodeo

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41

Wang, Jen-Yeu. "Human PC4 Prevents Mutagenesis and Killing by Oxidative DNA Damage: a Dissertation." eScholarship@UMMS, 2012. http://escholarship.umassmed.edu/gsbs_diss/287.

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Chapter II Abstract Human positive cofactor 4 (PC4) is a transcriptional coactivator with a highly conserved single-strand DNA (ssDNA) binding domain of unknown function. We identified PC4 as a suppressor of the oxidative mutator phenotype of the Escherichia coli fpg mutY mutant and demonstrate that this suppression requires its ssDNA binding activity. Saccharomyces cerevisiae mutants lacking their PC4 ortholog Sub1 are sensitive to hydrogen peroxide and exhibit spontaneous and peroxide-induced hypermutability. PC4 expression suppresses the peroxide sensitivity of the yeast sub1Δ mutant, sugge

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42

Eyre, Tina Ann. "Informatic analysis of proteins with a role in oxidative damage and ageing." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445475/.

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Ageing is a complex, universal process that remains very poorly understood, particularly in mammals. This thesis attempts to increase our understanding of ageing by predicting the structure of the uncoupling proteins, membrane proteins with a possible role in the modulation of oxidative damage, and therefore of ageing. A 3-dimensional model of the uncoupling proteins is generated, based on an analysis of known membrane proteins structures. In order to assess the accuracy of this model it is compared to the actual structure of a homologous protein, solved after the modelling was complete. A hom

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43

Bedi, Fernand Mel. "Synthesis and Fate of Oligonucleotides Containing the Oxidative Damage Product 3'-Oxothymidine." University of Toledo / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1429183009.

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Wang, Jen-Yeu. "Human PC4 Prevents Mutagenesis and Killing by Oxidative DNA Damage: a Dissertation." eScholarship@UMMS, 2004. https://escholarship.umassmed.edu/gsbs_diss/287.

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Chapter II Abstract Human positive cofactor 4 (PC4) is a transcriptional coactivator with a highly conserved single-strand DNA (ssDNA) binding domain of unknown function. We identified PC4 as a suppressor of the oxidative mutator phenotype of the Escherichia coli fpg mutY mutant and demonstrate that this suppression requires its ssDNA binding activity. Saccharomyces cerevisiae mutants lacking their PC4 ortholog Sub1 are sensitive to hydrogen peroxide and exhibit spontaneous and peroxide-induced hypermutability. PC4 expression suppresses the peroxide sensitivity of the yeast sub1Δ mutant, sugge

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45

Coombs, Anne-Marie. "A study of near-ultraviolet radiation induced oxidative damage in Escherichia coli." Thesis, University of Bath, 1988. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380929.

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46

Holbrook, Kailea J. Ms. "Effects of Acclimation on Temperature Tolerance and Oxidative Damage in Daphnia magna." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etd/3068.

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Freshwater zooplankton crustacean Daphnia frequently face strong temperature fluctuations in its natural environment, which necessitates adaptive plastic responses. This study focuses on changes in lipid peroxidation and total oxidative capacity in Daphnia tissues in response to long-term and short-term temperature changes. Long-term acclimation to 28ºC helped Daphnia survive longer at lethally high temperatures. This difference, however, was not accompanied by changes in lipid peroxidation, indicating that it isn’t a good measure of damage or predictor of temperature tolerance. On the other h

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47

Ghosh, Avik Kumar. "Charge migration and one-electron oxidation at adenine and thymidine containing DNA strands and role of guanine N1 imino proton in long range charge migration through DNA." Diss., Available online, Georgia Institute of Technology, 2007, 2007. http://etd.gatech.edu/theses/available/etd-05132007-000502/.

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Thesis (Ph. D.)--Chemistry and Biochemistry, Georgia Institute of Technology, 2008.<br>Wartell, Roger, Committee Member ; Bunz, Uwe, Committee Member ; Doyle, Donald, Committee Member ; Fahrni, Christoph, Committee Member ; Schuster, Gary, Committee Chair.

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48

Timms, Andrew Robert. "Spontaneous mutagenesis in stressed Escherichia coli." Thesis, Open University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244410.

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49

Wolfreys, Alison Mandy. "Molecular mutation spectra of 6-thioguanine resistant human T-lymphocyte and UV-irradiated lymphoblastoid mutants." Thesis, University of Sussex, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266549.

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50

Lassen, Natalie. "Roles of aldehyde dehydrogenases (ALDHs) against oxidative stress /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.

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Thesis (Ph.D. in Toxicology) -- University of Colorado at Denver and Health Sciences Center, 2006.<br>Typescript. Includes bibliographical references (leaves 119-138). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;

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