Relevant bibliographies by topics / Oxidative damage

Academic literature on the topic 'Oxidative damage'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 September 2023

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Journal articles on the topic "Oxidative damage"

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Krisko, Anita, and Miroslav Radman. "Protein damage, ageing and age-related diseases." Open Biology 9, no. 3 (March 2019): 180249. http://dx.doi.org/10.1098/rsob.180249.

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Ageing is considered as a snowballing phenotype of the accumulation of damaged dysfunctional or toxic proteins and silent mutations (polymorphisms) that sensitize relevant proteins to oxidative damage as inborn predispositions to age-related diseases. Ageing is not a disease, but it causes (or shares common cause with) age-related diseases as suggested by similar slopes of age-related increase in the incidence of diseases and death. Studies of robust and more standard species revealed that dysfunctional oxidatively damaged proteins are the root cause of radiation-induced morbidity and mortality. Oxidized proteins accumulate with age and cause reversible ageing-like phenotypes with some irreversible consequences (e.g. mutations). Here, we observe in yeast that aggregation rate of damaged proteins follows the Gompertz law of mortality and review arguments for a causal relationship between oxidative protein damage, ageing and disease. Aerobes evolved proteomes remarkably resistant to oxidative damage, but imperfectly folded proteins become sensitive to oxidation. We show that α-synuclein mutations that predispose to early-onset Parkinson's disease bestow an increased intrinsic sensitivity of α-synuclein to in vitro oxidation. Considering how initially silent protein polymorphism becomes phenotypic while causing age-related diseases and how protein damage leads to genome alterations inspires a vision of predictive diagnostic, prognostic, prevention and treatment of degenerative diseases.
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Nunomura, Akihiko, Kazuhiro Honda, Atsushi Takeda, Keisuke Hirai, Xiongwei Zhu, Mark A. Smith, and George Perry. "Oxidative Damage to RNA in Neurodegenerative Diseases." Journal of Biomedicine and Biotechnology 2006 (2006): 1–6. http://dx.doi.org/10.1155/jbb/2006/82323.

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Since 1999, oxidative damage to RNA molecules has been described in several neurological diseases including Alzheimer's disease, Parkinson's disease, Down syndrome, dementia with Lewy bodies, prion disease, subacute sclerosing panencephalitis, and xeroderma pigmentosum. An early involvement of RNA oxidation of vulnerable neuronal population in the neurodegenerative diseases has been demonstrated, which is strongly supported by a recent observation of increased RNA oxidation in brains of subjects with mild cognitive impairment. Until recently, little is known about consequences and cellular handling of the RNA damage. However, increasing body of evidence suggests detrimental effects of the RNA damage in protein synthesis and the existence of several coping mechanisms including direct repair and avoiding the incorporation of the damaged ribonucleotides into translational machinery. Further investigations toward understanding of the consequences and cellular handling mechanisms of the oxidative RNA damage may provide significant insights into the pathogenesis and therapeutic strategies of the neurodegenerative diseases.
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Rice-Evans, C., S. C. Omorphos, and E. Baysal. "Sickle cell membranes and oxidative damage." Biochemical Journal 237, no. 1 (July 1, 1986): 265–69. http://dx.doi.org/10.1042/bj2370265.

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Sickle erythrocytes and their membranes are susceptible to endogenous free-radical-mediated oxidative damage which correlates with the proportion of irreversibly sickled cells. The suppression of incubation-induced oxidative stress by antioxidants, free radical scavengers and an iron chelator suggest that oxidation products of membrane-bound haemoglobin contribute towards the pathology of the disease.
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Singh, Abhishek Kumar, Sandeep Singh, Geetika Garg, and Syed Ibrahim Rizvi. "Rapamycin alleviates oxidative stress-induced damage in rat erythrocytes." Biochemistry and Cell Biology 94, no. 5 (October 2016): 471–79. http://dx.doi.org/10.1139/bcb-2016-0048.

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An imbalanced cellular redox system promotes the production of reactive oxygen species (ROS) that may lead to oxidative stress-mediated cell death. Erythrocytes are the best-studied model of antioxidant defense mechanism. The present study was undertaken to investigate the effect of the immunosuppressant drug rapamycin, an inducer of autophagy, on redox balance of erythrocytes and blood plasma of oxidatively challenged rats. Male Wistar rats were oxidatively challenged with HgCl2 (5 mg/kg body mass (b.m.)). A significant (p < 0.05) induction in ROS production, plasma membrane redox system (PMRS), intracellular Ca2+ influx, lipid peroxidation (LPO), osmotic fragility, plasma protein carbonyl (PCO) content, and plasma advanced oxidation protein products (AOPP) and simultaneously significant reduction in glutathione (GSH) level and ferric reducing ability of plasma (FRAP) were observed in rats exposed to HgCl2. Furthermore, rapamycin (0.5 mg/kg b.m.) provided significant protection against HgCl2-induced alterations in rat erythrocytes and plasma by reducing ROS production, PMRS activity, intracellular Ca2+ influx, LPO, osmotic fragility, PCO content, and AOPP and also restored the level of antioxidant GSH and FRAP. Our observations provide evidence that rapamycin improves redox status and attenuates oxidative stress in oxidatively challenged rats. Our data also demonstrate that rapamycin is a comparatively safe immunosuppressant drug.
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Skrypnyk, N. V., and O. O. Maslova. "Oxidative DNA damage." Biopolymers and Cell 23, no. 3 (May 20, 2007): 202–14. http://dx.doi.org/10.7124/bc.000766.

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Davenport, R. J. "Trash Cache: Secret mitochondrial weapon fights oxidative damage (Oxidative damage)." Science of Aging Knowledge Environment 2002, no. 12 (March 27, 2002): 41nw—41. http://dx.doi.org/10.1126/sageke.2002.12.nw41.

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Sherman, Michael. "Oxidative Damage in Neurodegenerative Diseases: Relevance of Dietary Antioxidants." Neuroscience and Neurological Surgery 2, no. 5 (November 20, 2018): 01–03. http://dx.doi.org/10.31579/2578-8868/040.

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DAS, Nilanjana, Rodney L. LEVINE, William C. ORR, and Rajindar S. SOHAL. "Selectivity of protein oxidative damage during aging in Drosophila melanogaster." Biochemical Journal 360, no. 1 (November 8, 2001): 209–16. http://dx.doi.org/10.1042/bj3600209.

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The purpose of the present study was to determine whether oxidation of various proteins during the aging process occurs selectively or randomly, and whether the same proteins are damaged in different species. Protein oxidative damage to the proteins, present in the matrix of mitochondria in the flight muscles of Drosophila melanogaster and manifested as carbonyl modifications, was detected immunochemically with anti-dinitrophenyl-group antibodies. Aconitase was found to be the only protein in the mitochondrial matrix that exhibited an age-associated increase in carbonylation. The accrual of oxidative damage was accompanied by an approx. 50% loss in aconitase activity. An increase in ambient temperature, which elevates the rate of metabolism and shortens the life span of flies, caused an elevation in the amount of aconitase carbonylation and an accelerated loss in its activity. Exposure to 100% ambient oxygen showed that aconitase was highly susceptible to undergo oxidative damage and loss of activity under oxidative stress. Administration of fluoroacetate, a competitive inhibitor of aconitase activity, resulted in a dose-dependent decrease in the life span of the flies. Results of the present study demonstrate that protein oxidative damage during aging is a selective phenomenon, and might constitute a mechanism by which oxidative stress causes age-associated losses in specific biochemical functions.
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Anderson, Andrew P., Xuemei Luo, William Russell, and Y. Whitney Yin. "Oxidative damage diminishes mitochondrial DNA polymerase replication fidelity." Nucleic Acids Research 48, no. 2 (December 4, 2019): 817–29. http://dx.doi.org/10.1093/nar/gkz1018.

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Abstract Mitochondrial DNA (mtDNA) resides in a high ROS environment and suffers more mutations than its nuclear counterpart. Increasing evidence suggests that mtDNA mutations are not the results of direct oxidative damage, rather are caused, at least in part, by DNA replication errors. To understand how the mtDNA replicase, Pol γ, can give rise to elevated mutations, we studied the effect of oxidation of Pol γ on replication errors. Pol γ is a high fidelity polymerase with polymerase (pol) and proofreading exonuclease (exo) activities. We show that Pol γ exo domain is far more sensitive to oxidation than pol; under oxidative conditions, exonuclease activity therefore declines more rapidly than polymerase. The oxidized Pol γ becomes editing-deficient, displaying a 20-fold elevated mutations than the unoxidized enzyme. Mass spectrometry analysis reveals that Pol γ exo domain is a hotspot for oxidation. The oxidized exo residues increase the net negative charge around the active site that should reduce the affinity to mismatched primer/template DNA. Our results suggest that the oxidative stress induced high mutation frequency on mtDNA can be indirectly caused by oxidation of the mitochondrial replicase.
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Huang, Yue, Zhiling Li, En Lin, Pei He, and Gaizhen Ru. "Oxidative damage-induced hyperactive ribosome biogenesis participates in tumorigenesis of offspring by cross-interacting with the Wnt and TGF-β1 pathways in IVF embryos." Experimental & Molecular Medicine 53, no. 11 (November 2021): 1792–806. http://dx.doi.org/10.1038/s12276-021-00700-0.

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AbstractIn vitro fertilization (IVF) increases the risk of tumorigenesis in offspring. The increased oxidative damage during IVF may be involved in tumor formation. However, the molecular mechanisms underlying this phenomenon remain largely unclear. Using a well-established model of oxidatively damaged IVF mouse embryos, we applied the iTRAQ method to identify proteins differentially expressed between control and oxidatively damaged zygotes and explored the possible tumorigenic mechanisms, especially with regard to the effects of oxidative damage on ribosome biogenesis closely related to tumorigenesis. The iTRAQ results revealed that ribosomal proteins were upregulated by oxidative stress through the Nucleolin/β-Catenin/n-Myc pathway, which stimulated ribosomes to synthesize an abundance of repair proteins to correct the damaged DNA/chromosomes in IVF-derived embryos. However, the increased percentages of γH2AX-positive cells and apoptotic cells in the blastocyst suggested that DNA repair was insufficient, resulting in aberrant ribosome biogenesis. Overexpression of ribosomal proteins, particularly Rpl15, which gradually increased from the 1-cell to 8-cell stages, indicated persistent hyperactivation of ribosome biogenesis, which promoted tumorigenesis in offspring derived from oxidatively damaged IVF embryos by selectively enhancing the translation of β-Catenin and TGF-β1. The antioxidant epigallocatechin-3-gallate (EGCG) was added to the in vitro culture medium to protect embryos from oxidative damage, and the expression of ribosome-/tumor-related proteins returned to normal after EGCG treatment. This study suggests that regulation of ribosome biogenesis by EGCG may be a means of preventing tumor formation in human IVF-derived offspring, providing a scientific basis for optimizing in vitro culture conditions and improving human-assisted reproductive technology.
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Dissertations / Theses on the topic "Oxidative damage"

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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 endothelial cells was very weak and could be overcome by as little as 5 femtomol hydrogen peroxide per cell. The effects were directly related to the amount of H2O2 available to each cell, rather than the concentration. Exposure to relatively low amounts of H2O2 (<0.5 picomol/cell) led to reduced endothelial cell function including prostacyclin production and mitochondrial dehydrogenase activity, and inhibited cell migration and proliferation. The cells showed gradual, partial recovery from these damaging effects. At low amounts (0.1 to 0.5 picomol/cell) H2O2 induced endothelial cell apoptosis within 48 hours of the exposure. After this time, some of the surviving cells showed evidence of senescence and could remain in culture for up to 30 days. Senescence was accompanied by an increase in cytoplasmic volume and accumulation of lipofusion. Investigation of -galactosidase activity suggested that the increased enzyme expression was linked to cell cycle rather than senescence. In conclusion, endothelial cells are very sensitive to oxidative damage but the nature of the damage is related to the degree of oxidative stress. The effects of oxidative stress may play an important role in atherosclerotic and cardiovascular diseases.
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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 AD using quantitative/real-time polymerase chain reaction (qPCR/ RT-PCR). To further test the hypothesis that diminished DNA repair capacity in the progression of AD contributes to increased DNA oxidation we will use custom PCR arrays and qPCR, Western blot analysis and activity assays to quantify changes in enzymes involved in base excision repair (BER). In order to carry out these studies tissue specimens from superior and middle temporal gyri (SMTG) and inferior parietal lobe (IP), as well as, a non-vulnerable region, the cerebellum (CER) will be analyzed from normal control (NC) subjects and subjects throughout the progression of AD including those with preclinical AD (PCAD), mild cognitive impairment (MCI), and late stage AD (LAD). We will also analyze specimens from diseased control subjects (DC; Frontotemporal dementia (FTD) and dementia with Lewy bodies (DLB)) to determine if the changes we observe in AD are specific.
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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 study describes the establishment of sensitive and specific techniques to chemically characterise and quantitate three markers of oxidative DNA damage, namely: cis-thymine glycol (Tg), 5-hydroxymethyluracil (5-OHMeU) and 8-hydroxyguanine (8-OHG). Techniques using gas chromatography/mass spectrometry (GC/MS) were established for Tg and 5-OHMeU, following their derivatisation with N-methyl-N-(tert-butyldimethylsilyl) trifluoroacetamide (MTBSTFA). Standards of Tg and 5-OHMeU were synthesised, and stable isotopically labelled analogues were prepared as internal standards. Analysis of the DNA was carried out at the base level and therefore required acidic hydrolysis of the DNA in order to release the modified and intact bases. For the quantitation of 8-OHG a novel procedure using high performance liquid chromatography (HPLC) - electrochemical detection (ECD) with guanase incubation of DNA hydrolysates was established. The established assays were used to quantitate DNA lesions in vitro and in vivo. In vitro dose response curves were established for the three markers upon gamma-irradiation of DNA. In vivo results of an animal inhalation study indicated there was not a significant increase in oxidative damage upon exposure to crocidolite. An antioxidant supplementation study in humans placental DNA also did not show a significant reduction in levels of the three markers upon supplementation. Comparable background levels of Tg and 5-OHMeU were observed in human and calf thymus DNA, while 8-OHG levels were found to be significantly higher.
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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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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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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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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.
Includes bibliographical references (p. 209-222).
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 occasionally consid­ered as a "quality concern" since it rarely detectable using standard biochemical techniques. The production of an oxidatively-sensitive protein, a1-Antitrypsin, was investigated to ascertain the effect of fermentation parameters on the extent of oxidation. Oxidation of either of two methion­ine residues in the active site to methionine sulfoxide was sufficient for inactivation, and 50% of the antitrypsin produced under standard fermentation conditions was oxidized. Oxidative damage was linked to the dissolved oxygen concentration by experimentation and detailed modeling of the evolution and detoxification of reactive oxygen species. Under pseudo steady-state conditions, the fractional oxidation is near zero under anaerobic conditions and increases through the microaero­bic regime. At dissolved oxygen concentrations greater than 10% of air saturation, the fractional oxidation did not vary. Step changes in the dissolved oxygen concentration, designed to emulate possible time variation resulting from poor mixing or changes in gas composition, caused tran­sient increases in the fractional oxidation and enhanced proteolytic degradation. This may impli­cate oxidative stress in scale-up related protein quality and quantity limitations. In addition, oxidative damage to antitrypsin caused a 5-fold increase in the stepwise addition rate for in vitro aggregation, which suggests that oxidative damage will limit shelf stability. In addition, process simulation demonstrated that removal of oxidative variants caused a 100% increase in cost per unit when only 22% of the antitrypsin is oxidized during the fermentation step.
by John O. Konz.
Ph.D.
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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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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 between MPO-derived oxidants and selenium compounds were determined product characterization of products performed. The reduction of the oxidised products, selenoxides, was examined and the rate constant for the thiol reduction of selenoxides determined. It is demonstrated that selenium and sulfur containing enzymes are capable of scavenging these oxidants, as well as reversing the formation of selenoxides. The ability of selenium compounds to protect against damage induced by treatment of cells with HOCl and N-chloramines was also assessed. Overall, selenium containing compounds and enzymes show potential in scavenging these oxidants with endogenous thiols capable of reversing the oxidised selenium products, making them a potential therapeutic intervention in inflammatory conditions.
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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 several cationic lipids with various lengths of dialkyl chain (2, 8, 18) and spermine (Sp4+) binding core in this research, which posses strong DNA binding affinity due to their multi-charged spermine head-groups. Among those, C8GlySp4+ and C2GlySp4+ can form stable complex with DNA oligomer in aqueous solution, characterized by time dependent UV and CD spectrometry. C2GlySp4+ showed the similar inhibition on oxidative damage in GG steps as spermine while C8GlySp4+ demonstrated much more significant prohibitive effect at the same concentration. Since all the lipids bear the same binding core, they should afford the similar binding affinity towards DNA duplexes. we attributed the observation to the longer length of dialkyl group in C8GlySp4+, which can more effectively shield the DNA duplex from the water molecules than either spermine or C2GlySp4+. A kinetic model based on phonon-assist polaron hopping mechanism was proposed to rationalize the experimental results. The finding may give insight on the protection of DNA oxidative damage by reducing the access of the water molecule to DNA duplex and may have potential impact on the application of DNA as conducting biopolymer and protection of DNA in biological system.
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Books on the topic "Oxidative damage"

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Evans, Mark D., and Marcus S. Cooke, eds. Oxidative Damage to Nucleic Acids. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-72974-9.

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1962-, Evans Mark D., and Cooke Marcus S, eds. Oxidative damage to nucleic acids. Austin, Tex: Landes Bioscience, 2007.

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Connor, James R., ed. Metals and Oxidative Damage in Neurological Disorders. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0197-2.

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R, Connor James, ed. Metals and oxidative damage in neurological disorders. New York: Plenum Press, 1997.

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Gadoth, Natan, and Hans Hilmar Göbel, eds. Oxidative Stress and Free Radical Damage in Neurology. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60327-514-9.

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Hannon-Fletcher, Mary Philomena Anne. Oxidative stress and biomolecule damage in human IDDM. [S.l: The Author], 1999.

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J, Jesaitis Algirdas, Dratz Edward A, and Montana State University (Bozeman, Mont.), eds. The molecular basis of oxidative damage by leukocytes. Boca Raton: CRC Press, 1992.

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J, Lunec, ed. Measuring in vivo oxidative damage: A practical approach. Chichester: Wiley, 2000.

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Beal, M. Flint. Mitochondrial dysfunction and oxidative damage in neurodegenerative diseases. Austin: R.G. Landes Co., 1995.

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-H, Goebel H., ed. Oxidative stress and free radical damage in neurology. New York: Humana Press, 2011.

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Book chapters on the topic "Oxidative damage"

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Guengerich, F. Peter. "Oxidative DNA Damage." In Molecular Life Sciences, 1–7. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-6436-5_441-1.

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Collins, Andrew R. "Oxidative DNA Damage." In Encyclopedia of Cancer, 2728–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4306.

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Guengerich, Frederick Peter. "Oxidative DNA Damage." In Molecular Life Sciences, 849–54. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-1531-2_441.

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"Oxidative Damage." In Encyclopedia of Biophysics, 1813. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-16712-6_100715.

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Balin, A. K., and M. Vilenchik. "Oxidative Damage." In Encyclopedia of Gerontology, 303–10. Elsevier, 2007. http://dx.doi.org/10.1016/b0-12-370870-2/00144-x.

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STERN, ARNOLD. "Red Cell Oxidative Damage." In Oxidative Stress, 331–49. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-12-642760-8.50018-1.

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Borek, Carmia. "CANCER AND OXIDATIVE STRESS." In Oxidative Damage & Repair, 762–66. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-08-041749-3.50138-8.

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Floyd, Robert A. "DNA DAMAGE AND REPAIR." In Oxidative Damage & Repair, 175–80. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-08-041749-3.50036-x.

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Stadtman, E. R. "PROTEIN DAMAGE AND REPAIR." In Oxidative Damage & Repair, 348–54. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-08-041749-3.50066-8.

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Sevanian, Alex. "LIPID DAMAGE AND REPAIR." In Oxidative Damage & Repair, 543–49. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-08-041749-3.50100-5.

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Conference papers on the topic "Oxidative damage"

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Shikov, A. E., V. V. Lastochkin, T. V. Chirkova, and V. V. Emelyanov. "Oxidative damage to plant lipids and proteins bynatural and artificial oxidative stress." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-481.

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Watson, Walter Philip, Carl W. Aften, and David J. Previs. "Delayed-Release Coatings for Oxidative Breakers." In SPE International Symposium and Exhibition on Formation Damage Control. Society of Petroleum Engineers, 2010. http://dx.doi.org/10.2118/127895-ms.

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Bonetta, Sa, V. Gianotti, D. Scozia, Si Bonetta, E. Carraro, F. Gosetti, M. Oddone, and M. C. Gennaro. "Genotoxic and oxidative damage related to PM2.5chemical fraction." In AIR POLLUTION 2008. Southampton, UK: WIT Press, 2008. http://dx.doi.org/10.2495/air080551.

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Xuena Zhu, P. Shah, and Chenzhong Li. "Paper-based Immunosensor for Oxidative DNA Damage Biomarker Detection." In 2013 29th Southern Biomedical Engineering Conference (SBEC 2013). IEEE, 2013. http://dx.doi.org/10.1109/sbec.2013.71.

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Ding, Ning, Sam Miller, and Heather O'Hagan. "Abstract 5317: JAK2 regulates oxidative damage-induced epigenetic alterations." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5317.

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Tekutskaya, E. E., and I. S. Raybova. "OXIDATIVE DAMAGE TO DNA, IONIZING RADIATION AND MAGNETIC FIELDS." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.21.

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In this work, we studied the mechanisms of damage to the structure of DNA extracted from human whole blood after exposure to blood samples of various types of ionizing radiation and a lowfrequency magnetic field. Oxidative damage of nitrogenous bases and single-stranded DNA breaks are caused by the formation of reactive oxygen species generated by radiation.
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Bennet, Devasier, and Sanghyo Kim. "ECIS to assess human skin cell photo-oxidative damage." In 2013 International Conference on Advanced Nanomaterials and Emerging Engineering Technologies (ICANMEET). IEEE, 2013. http://dx.doi.org/10.1109/icanmeet.2013.6609393.

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Pietrangeli, Emanuele, Filippo Cappuccini, Michelangelo Bellacci, Federico Iozzelli, and Marco Romanelli. "Characterization and Oxidation Damage Modelling of MCrAlY." In ASME Turbo Expo 2006: Power for Land, Sea, and Air. ASMEDC, 2006. http://dx.doi.org/10.1115/gt2006-90138.

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Overlay coatings based on the MCrAlY alloy system (M is Ni, CO or both) are among the most important protective coating materials applied in the hottest section of gas turbine to counteract hot corrosion and high temperature oxidation. MCrAlY coatings are arranged in γ/β-phase system, where β-phase is the Al reserve for the surface oxide layer formation. Like any coating designed to resist oxidative environments at high temperatures, MCrAlYs should be capable of developing a thermodynamically stable, slow-growing and adherent surface oxide layer. In the current paper, two HVOF thermal sprayed MCrAlYs deposited on a Ni-based superalloy have been investigated in order to assess the different high temperature oxidation resistance. Isothermal oxidation tests were performed on NiCoCrAlY coating (GT33®) and CoNiCrAlY coating (Amdry995®) at four temperatures for thousand hours. Coating damage was evaluated by measures of outer and inner β-phase depletion, interdiffusion zone thickness and Al reduction. Both coatings have shown optimal microstructural stability but NiCoCrAlY coating, in virtue of greater Ni and Al content, proved superior high temperature oxidation resistance. A useful model for life assessment of gas turbine buckets coatings was extrapolated from microstructure evolution data.
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Chen, Xiaolian, Linzhi Gong, and Jianxiong Xu. "Probiotics Attenuate Sperm Damage Induced by Oxidative Stress in Rats." In 2012 International Conference on Biomedical Engineering and Biotechnology (iCBEB). IEEE, 2012. http://dx.doi.org/10.1109/icbeb.2012.314.

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Madenci, Erdogan, and Selda Oterkus. "Peridynamic Modeling of Thermo-Oxidative Damage Evolution in a Composite Lamina." In 58th AIAA/ASCE/AHS/ASC Structures, Structural Dynamics, and Materials Conference. Reston, Virginia: American Institute of Aeronautics and Astronautics, 2017. http://dx.doi.org/10.2514/6.2017-0197.

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Reports on the topic "Oxidative damage"

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Beal, M. F. Oxidative Damage in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada434051.

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Beal, M. F. Oxidative Damage in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada416957.

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Goth-Goldstein, Regine. Oxidative Damage, CYP1B1 and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada409396.

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Browne, Susan E. Bioenergetic Defects and Oxidative Damage in Transgenic Mouse Models of Neurodegenerative Disorders. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada430585.

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Goodwin, Edwin H. Biological Effects of LLIR and Normal Oxidative Damage: The Same or Different? Office of Scientific and Technical Information (OSTI), June 2000. http://dx.doi.org/10.2172/833474.

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Browne, Susan E. Bioenergetic Defects and Oxidative Damage in Transgenic Mouse Models of Neurodegenerative Disorders. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada419306.

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Browne, Susan E. Bioenergetic Defects and Oxidative Damage in Transgenic Mouse Models of Neurodegenerative Disorders. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada460659.

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Wu, Guangyu. Preventive Role of Specific Dietary Factors and Natural Compounds Against DNA Damage and Oxidative Stress. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada377925.

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Barragan Echenique, Diego. ?-TEA?s Tumor Toxicity may be Attributed to its Capability of Inducing Oxidative Damage in the Endoplasmic Reticulum. Portland State University Library, January 2015. http://dx.doi.org/10.15760/honors.172.

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Wen, Qin, Xueqin Hong, Kunze He, and Min Li. Can acupuncture reverse oxidative stress and neuroinflammatory damage in animal models of vascular Dementia? A preclinical systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2023. http://dx.doi.org/10.37766/inplasy2023.3.0114.

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