Thematische Bibliographien / DNA Effect of radiation on

Inhaltsverzeichnis

  1. Zeitschriftenartikel
  2. Dissertationen
  3. Bücher
  4. Buchteile
  5. Konferenzberichte
  6. Berichte der Organisationen

Auswahl der wissenschaftlichen Literatur zum Thema „DNA Effect of radiation on“

Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 1. Februar 2022

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Zeitschriftenartikel zum Thema "DNA Effect of radiation on"

1

Jalal, Nasir, Saba Haq, Namrah Anwar, Saadiya Nazeer und Umar Saeed. „Radiation induced bystander effect and DNA damage“. Journal of Cancer Research and Therapeutics 10, Nr. 4 (2014): 819. http://dx.doi.org/10.4103/0973-1482.144587.

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2

Kalinich, John F., George N. Catravas und Stephen L. Snyder. „The Effect of γ Radiation on DNA Methylation“. Radiation Research 117, Nr. 2 (Februar 1989): 185. http://dx.doi.org/10.2307/3577319.

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3

Rita, Ghosh, und Hansda Surajit. „Targeted and non-targeted effects of radiation in mammalian cells: An overview“. Archives of Biotechnology and Biomedicine 5, Nr. 1 (12.04.2021): 013–19. http://dx.doi.org/10.29328/journal.abb.1001023.

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Radiation of different wavelengths can kill living organisms, although, the mechanism of interactions differs depending on their energies. Understanding the interaction of radiation with living cells is important to assess their harmful effects and also to identify their therapeutic potential. Temporally, this interaction can be broadly divided in three stages – physical, chemical and biological. While radiation can affect all the important macromolecules of the cells, particularly important is the damage to its genetic material, the DNA. The consequences of irradiation include- DNA damage, mutation, cross-linkages with other molecules, chromosomal aberrations and DNA repair leading to altered gene expression and/or cell death. Mutations in DNA can lead to heritable changes and is important for the induction of cancer. While some of these effects are through direct interaction of radiation with the target, radiation can interact with the surrounding environment to result in its indirect actions. The effects of radiation depend not only on the total dose but also on the dose rate, LET etc. and also on the cell types. However, action of radiation on organisms is not restricted to interactions with irradiated cells, i.e. target cells alone; it also exerts non-targeted effects on neighboring unexposed cells to produce productive responses; this is known as bystander effect. The bystander effects of ionizing radiations are well documented and contribute largely to the relapse of cancer and secondary tumors after radiotherapy. Irradiation of cells with non-ionizing Ultra-Violet light also exhibits bystander responses, but such responses are very distinct from that produced by ionizing radiations.
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Yokoya, A., N. Shikazono, K. Fujii, A. Urushibara, K. Akamatsu und R. Watanabe. „DNA damage induced by the direct effect of radiation“. Radiation Physics and Chemistry 77, Nr. 10-12 (Oktober 2008): 1280–85. http://dx.doi.org/10.1016/j.radphyschem.2008.05.021.

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5

Georgakilas, Alexandros G. „Role of DNA Damage and Repair in Detrimental Effects of Ionizing Radiation“. Radiation 1, Nr. 1 (22.10.2020): 1–4. http://dx.doi.org/10.3390/radiation1010001.

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Ionizing radiation (IR) is considered a traditional mutagen and genotoxic agent. Exposure to IR affects in all cases biological systems and living organisms from plants to humans mostly in a pernicious way. At low (<0.1 Gy) and low-to-medium doses (0.1–1 Gy), one can find in the literature a variety of findings indicating sometimes a positive-like anti-inflammatory effect or detrimental-like toxicity. In this Special Issue and in general in the current research, we would like to acquire works and more knowledge on the role(s) of DNA damage and its repair induced by ionizing radiations as instigators of the full range of biological responses to radiation. Emphasis should be given to advances offering mechanistic insights into the ability of radiations with different qualities to severely impact cells or tissues. High-quality research or review studies on different species projected to humans are welcome. Technical advances reporting on the methodologies to accurately measure DNA or other types of biological damage must be highly considered for the near future in our research community, as well. Last but not least, clinical trials or protocols with improvements to radiation therapy and radiation protection are also included in our vision for the advancement of research regarding biological effects of IR.
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Turaeva, N. N., S. Schroeder und B. L. Oksengendler. „Effect of Anderson Localization on Auger Destruction of DNA“. ISRN Biophysics 2012 (05.12.2012): 1–3. http://dx.doi.org/10.5402/2012/972085.

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The effect of Anderson localization in DNA on the Auger destruction by the Coulombic explosion at ionized radiation has been theoretically discussed in the present work. The theory of Auger destruction of DNA has been modified taking into account the localized and delocalized electron states in DNA owing to the correlated disorder in a sequence of nucleotides. According to the modified theoretical model of Auger destruction, the dominant ratio of delocalized states to localized states in exon compared to intron results in stronger radiation resistance of exons to ionized irradiation causing the Auger-cascade process than the radiation resistance of introns.
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Ganeva, Roumiana L., und Lyuben M. Tzvetkov. „Effect of Cisplatin Alone and in Combination with γ-Radiation on the Initiation of DNA Synthesis in Friend Leukemia Cells“. Zeitschrift für Naturforschung C 52, Nr. 5-6 (01.06.1997): 405–7. http://dx.doi.org/10.1515/znc-1997-5-620.

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The effect of the anticancer drug cisplatin (alone and in combination with γ-radiation) on the initiation of DNA synthesis in Friend leukemia cells was studied. A method for isolation of DNA fractions containing the origins of replication was used. It was found that cisplatin decreased the rate of the initiation of DNA synthesis. The mild γ-radiation has previously been observed to inhibit the initiation of DNA synthesis. In the present investigation the combination of cisplatin and γ-radiation showed additive effects without synergism on the initiation of DNA biosynthesis.
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Greubel, Christoph, Volker Hable, Guido A. Drexler, Andreas Hauptner, Steffen Dietzel, Hilmar Strickfaden, Iris Baur et al. „Competition effect in DNA damage response“. Radiation and Environmental Biophysics 47, Nr. 4 (23.07.2008): 423–29. http://dx.doi.org/10.1007/s00411-008-0182-z.

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Bangruwa, Neeraj, Manish Srivastava und Debabrata Mishra. „Radiation-Induced Effect on Spin-Selective Electron Transfer through Self-Assembled Monolayers of ds-DNA“. Magnetochemistry 7, Nr. 7 (08.07.2021): 98. http://dx.doi.org/10.3390/magnetochemistry7070098.

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Stability of the DNA molecule is essential for the proper functioning and sustainability of all living organisms. In this study, we investigate the effect of gamma radiation (γ-radiation) on spin-selective electron transfer through double strand (ds)DNA molecules. Self-assembled monolayers (SAMs) of 21-base long DNA are prepared on Au-coated Ni thin film. We measure the spin polarization (%) of the SAMs of ds-DNA using the spin-dependent electrochemical technique. We use a Cs-based γ-radiation source to expose the SAMs of ds-DNA immobilized on thin films for various time intervals ranging from 0–30 min. The susceptibility of DNA to γ-radiation is measured by spin-dependent electrochemistry. We observe that the efficiency of spin filtering by ds-DNA gradually decreases when exposure (to γ-radiation) time increases, and drops below 1% after 30 min of exposure. The change in spin polarization value is related either to the conformational perturbation in DNA or to structural damage in DNA molecules caused by ionizing radiation.
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rezaiekahkhaie, sakine, und Khadije Rezaie Keikhaie. „The Role of Ionizing Radiation in Cellular Signaling Pathways, Mutagenesis, and Carcinogenesis“. International Journal of Basic Science in Medicine 3, Nr. 4 (13.01.2019): 147–53. http://dx.doi.org/10.15171/ijbsm.2018.26.

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One of the negative effects of ionizing radiation is the alteration of cellular signaling pathways which lead to carcinogenesis and tumorigenesis. In this review, we discussed the impacts of ionizing radiation on cells and cellular signaling pathways. In this regard, exposure to radiation can directly or indirectly alter cellular signaling pathways. Remarkably, irradiated cells release special mediators into cellular matrix, aberrating cell-cell and cell-environment interactions. Most notably, these mediators include nitric oxide (NO), reactive oxygen species (ROS), and cell growth factors which contribute to cellular interactions between irradiated cells and their neighbor cells, a phenomenon known as radiation-induced bystander effect. DNA molecule is the most important cellular compartment damaged by ionizing radiation. On the other hand, the ability of irradiated cells to repair the damaged DNA is very low. Therefore, DNA alternations are passed to the next generations, and ultimately lead to carcinogenesis. The study of ionizing radiations and their impacts on biological systems is of remarkable importance to divulge their impacts on cellular signaling pathways.
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Dissertationen zum Thema "DNA Effect of radiation on"

1

MacPhail, Susan Helen. „Effect of intercellular contact on radiation-induced DNA damage“. Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27986.

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Chinese hamster V79-171B cells grown for about 24 hours in suspension culture display increased resistance to cell killing by ionizing radiation compared with cells grown as monolayers, an observation originally termed the "contact effect". More recently, development of that resistance was shown to be accompanied by changes in the conformation of the DNA which reduce its denaturation rate in high salt/weak alkali. These changes in DNA conformation, mediated by the cellular micro-environment, appear to be responsible for the contact effect. The conditions necessary for the development of the effect are not, however, completely understood. In particular, when cells grown as monolayers on petri plates are suspended in spinner culture flasks, their growth characteristics change in three distinct ways. First, cells in suspension no longer have a solid substrate, so they remain round. Second, after several hours, they begin to aggregate to form "spheroids", so that three-dimensional intercellular cell contact develops. Third, cells in the stirred suspension cultures are not subjected to high local concentrations of metabolic by-products or surrounded by a zone depleted of nutrients, as are cells in monolayer culture. The studies described here were designed to determine how each of these factors influence changes in DNA conformation, as assayed using the alkali unwinding technique. Our results indicated that a round shape may not be an essential requirement, since cells spread out on the surface of cytodex beads in suspension culture, and sparsely-seeded cells in monolayer culture demonstrated at least a partial contact effect. Three-dimensional intercellular contact does not always seem necessary for the development of the contact effect. Cells grown in a methyl cellulose matrix developed radioresistance, even though the cells formed only small clusters of less than five cells. Similarly, suspension culture cells which were prevented from aggregating by frequent exposure to trypsin, also developed the contact effect. There was no evidence that nutrient depletion plays a role in the failure of cells grown as monolayers to develop a contact effect. However, cells grown as spheroids in the presence of monolayer cells, or in monolayer cell-conditioned medium, did not display a full contact effect. This indicates a role for monolayer cell-produced factors (possibly extracellular matrix proteins) in preventing the development of the contact effect. We conclude that changes in DNA conformation and the increase in radiation resistance, seen in V79-171b cells grown as spheroids, are not the result of intercellular contact or round shape of the cells. This radioresistance appears to be the result of an absence of monolayer cell-produced factors which could control both cell shape and DNA conformation.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Bajinskis, Ainars. „Studies of DNA repair strategies in response to complex DNA damages“. Doctoral thesis, Stockholms universitet, Institutionen för genetik, mikrobiologi och toxikologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-72472.

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The main aim of this thesis was to study the role of the indirect actions of γ-rays and α-particles on the complexity of primary DNA damages and the repair fidelity of major DNA repair pathways: non-homologous end joining (NHEJ), homologous recombination repair (HRR) and base excision repair (BER). The complexity of radiation-induced damages increases and the proximity between damages decreases with increasing LET due to formation of ionization clusters along the particle track. The complexity of damages formed can be modified by the free radical scavenger dimethyl sulfoxide (DMSO). In addition, the effects of low doses of low dose rate γ-radiation on cellular response in terms of differentiation were investigated. Paper I investigates the role of the indirect effect of radiation on repair fidelity of HRR, NHEJ and BER when damages of different complexity were induced by radiation or by potassium bromate. We found that potassium bromate induces complex DNA damages through processing of base modifications and that the indirect effect of radiation has a high impact on the NHEJ pathway. Results in paper II confirmed our conclusions in paper I that the indirect effect from both γ-rays and α-particles has an impact on all three repair pathways studied and NHEJ benefits the most when the indirect effect of radiation is removed. In paper III we investigated the effects of low dose/dose rate γ-radiation on the developmental process of neural cells by using cell models for neurons and astrocytes. Our results suggest that low dose/dose rate γ-radiation attenuates differentiation and down-regulates proteins involved in the differentiation process of neural cells by an epigenetic rather than cytotoxic mechanism.

At the time of doctoral defense, the following paper was unpublished and had a status as follows: Paper 2: Manuscript.

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Morabito, Brian Joseph. „Quantitating radiation induced DNA breaks by capillary electrophoresis“. Thesis, Georgia Institute of Technology, 1997. http://hdl.handle.net/1853/16339.

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Braddock, M. „Effects of radiation on DNA“. Thesis, University of Salford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356177.

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5

Verma, Meera Mary. „On the effect of UV-irradiation on DNA replication in Escherichia coli“. Title page, contents and summary only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09phv522.pdf.

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Byrne, Shaun Edward. „An investigation into the processing of ionising radiation induced clustered DNA damage sites using mammalian cell extracts“. Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670082.

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7

Roos, Wynand Paul. „The influence of DNA damage, DNA repair and chromatin structure on radiosensitivity“. Thesis, Stellenbosch : Stellenbosch University, 2001. http://hdl.handle.net/10019.1/52540.

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Thesis (PhD)--Stellenbosch University, 2001.
ENGLISH ABSTRACT: The factors which control radiosensitivity are of vital importance for the understanding of cell inactivation and for cancer therapy. Cell cycle blocks, total induced DNA damage, DNA repair, apoptosis and chromatin structure are likely to playa role in the responses leading to cell death. I have examined aspects of irradiation-induced G2/M blocks in DNA damage and repair. In HT29, L132 and ATs4 cells the total amount of induced DNA damage by isodoses of 4.5 Gy, 5 Gy and 2 Gy was found to be 14 %, 14 % and 12 % respectively. Most of the DNA repair was completed before the G2/M maximum and only 3 % of DNA damage remains to be restored in the G2/M block. The radiosensitivity in eleven cell lines was found to range from SF2 of 0.02 to 0.61. By FADU assay the undamaged DNA at 5 Gy was found to range from 56% to 93%. The initial DNA damage and radiosensitivity were highly correlated (r2=0. 81). After 5 Gy irradiation and 12 hours repair two groups of cell lines emerged. The group 1 cell lines restored undamaged DNA to a level ranging from 94 % to 98 %. The group 2 cell lines restored the undamaged DNA to a level ranging from 77 % to 82 %. No correlation was seen between residual DNA damage remaining after 12 hours repair and radiosensitivity. In CHO-K1 cells chromatin condensation induced by Nocodazole was found to marginally increase the radiosensitivity as shown by the change of the mean inactivation dose (D) from 4.446 to 4.376 Gy. Nocodazole also increased the initial DNA damage, induced by 5 Gy, from 7 % to 13 %. In xrs1 cells these conditions increased the radiosensitivity from D of 1.209 to 0.7836 Gy and the initial DNA damage from 43 % to 57 %. Disruption of chromatin structure with a hypertonic medium was found to increase radiosensitivity in CHO-K1 cells from D of 4.446 to 3.092 Gy and the initial DNA damage from 7 % to 15 %. In xrs1 cells these conditions caused radiosensitivity to decrease from D of 1.209 to 1.609 Gy and the initial DNA damage from 43 % to 36 %. Repair inhibition by Wortmannin increased the radiosensitivity in CHO-K1 from a D of 5.914 Gy in DMSO controls to a D 3.043 Gy. In xrs1 cells repair inhibition had no effect on radiosensitivity. Significant inhibition of repair was seen in CHO-K1 at 2 hours (p<0.0001) and at 20 hours (p=0.0095). No inhibition of repair was seen in xrs1 cells at 2 hours (p=0.6082) or 20 hours (p=0.6069). While DNA repair must be allocated to the post-irradiation period, the G2/M block seen in p53 mutants reaches a maximum only 12 hours post-irradiation when most of the repair is completed. As the G2/M block resolves and cells reenter cycle 28 hours after the G2 maximum it appears that repair processes cannot be the only reason for the G2IM cell cycle arrest. At low doses of irradiation initial DNA damage correlates with radiosensitivity. This suggests that the initial DNA damage is a determinant for radiosensitivity. Repair of DNA double-strand breaks by the non-homologous end joining (NHEJ) mechanism, identified by inhibition with Wortmannin, was shown to influence residual DNA damage and cell survival. Both the initial DNA damage and DNA repair were found to be influenced by chromatin structure. Chromatin structure was modulated by high salt and by Nocodazole, and has heen identified as a parameter which influences radiosensitivity.
AFRIKAANSE OPSOMMING: Die faktore wat betrokke is in die meganisme van stralings-sensitisering is van hoogs belang vir die begrip van sel inaktiveering en kanker terapie. Sel siklus blokke, totale geïnduseerde DNS skade, DNS herstel, apoptose en chromatien struktuur is moontlike rol vertolkers in die sellulêre response wat ly tot seldood. Ek het die aspekte van stralings-geïnduseerde G2/M blokke in DNS skade en DNS herstelondersoek. Die hoeveelheid geïnduseerde DNS skade, deur ooreenstemmende stralings-dosisse, in HT29, L132 en ATs4 selle is 14 %, 14 % en 12 %. Meeste van die DNS herstel is klaar voordat die G2/M maksimum beryk word en net 3 % DNS skade blyoor om herstel te word in die G2/M blok. Die stralings-sensitiwiteit in elf sel lyne varieer tussen 'n SF2 van 0.02 en 0.61. Deur die gebruik van die FADU metode is gevind dat die onbeskadigde DNS na 5 Gy bestraling varieer tussen 56 % en 93 %. Die totale geïnduseerde DNS skade en stralings-sensitiwiteit was hoogs gekorreleer (r2=0.81). Na 5 Gy bestraling en 12 ure herstel kan die sel lyne in twee groepe gegroepeer word. Die groep 1 sellyne herstel die onbeskadigde DNS terug na 'n vlak wat varieer tussen 94 % en 98 %. Die groep 2 sel lyne herstel die onbeskadigde DNS terug tot op 'n vlak wat varieer tussen 77 % en 82 %. Geen korrelasie is gesien tussen oorblywende DNS skade en stralings-sensitiwiteit na 12 ure herstel nie. In die CHO-K1 sel lyn, chromatien kompaksie geïnduseer deur Nocodazole, vererger die stralings- sensitiwiteit soos gesien deur die gemiddelde inaktiveerings dosis (D) wat verlaag het van 4.446 tot 4.376. Nocodazole het ook die totale DNS skade verhoog van 7 % tot 13 %. Onder dieselfde kondisies, in die xrs1 sel lyn, is 'n verergering van stralings-sensitiwiteit (D) gesien van 1.209 tot 0.7836 en verhoog ONS skade van 43 % tot 57 %. Die ontwrigting van die chromatien struktuur deur die gebruik van hipertoniese medium het die stralings-sensitiwiteit (D) vererger in CHO-K1 selle van 4.446 tot 3.092. Die totale ONS skade is verhoog van 7 % tot 15 %. Onder dieselfde kondisies, in die xrs1 sellyn, verbeter die stralings-sensitiwiteit (D) van 1.209 tot 1.609 en die totale ONS skade verminder van 43 % tot 36 %. ONS herstel inaktiveering in die teenwoordigheid van Wortmannin het die stralings-sensitiwiteit (D) in CHO-K1 selle vererger van 5.914 in DMSO verwysings kondisies tot 3.043. Die ONS herstel inaktiveering in xrs1 selle het geen uitwerking gehaat op stralingssensitiwiteit nie. Noemenswaardige inaktiveering van ONS herstel is gesien in CHO-K1 selle na 2 ure (p<0.0001) en na 20 ure (p=0.0095). Geen inaktiveering is gesien in xrs1 selle na 2 ure (p=0.6082) of na 20 ure (p=0.6069) nie. TerwylONS herstel moet plaasvind na die bestralings periode, beryk die G2/M blok in p53 gemuteerde selle sy maksimum 12 ure na bestraling terwyl meeste van die ONS herstel alreeds voltooi is. Aangesien die G2/M blok eers 28 ure later begin sirkuleer moet die G2/M blok nog 'n funksie vervul anders as ONS herstel. By lae dosisse van bestraling korreleer die totale geïnduseerde ONS skade met stralings-sensitiwiteit. Dit dui daarop dat die totale ONS skade 'n bepalende faktor moet wees in stralings-sensitiwiteit. Die herstel van ONS skade deur die nie-homoloë eindpunt samevoeging (NHES) meganisme, geïdentifiseer deur inaktiveering deur Wortmann in, het 'n invloed op oorblywende ONS skade en sellulêre oorlewing. Beide die totale ONS skade en ONS herstel was beïnvloed deur die chromatien struktuur. Chromatien struktuur was gemoduleer deur hoë sout konsentrasies en deur Nocodazole, en is geïdentifiseer as a belangrike parameter wat stralings-sensitiwiteit beïnvloed.
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Starrs, Sharon Margaret. „Molecular mechanisms of DNA photodamage“. Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314222.

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Sweeney, Marion Carol. „The effects of gamma radiation on DNA“. Thesis, University of Leicester, 1986. http://hdl.handle.net/2381/33943.

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Elsy, David. „The effects of gamma-radiation on DNA“. Thesis, University of Leicester, 1991. http://hdl.handle.net/2381/33664.

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In this study gamma-radiation-induced DNA strand breaks have been investigated using two systems: a plasmid-based assay, and a whole nuclei-, or whole cell-based, alkaline filter elution assay. Addition of alkali metal halides to DNA irradiated under frozen aqueous conditions were observed to have an effect on the radiosensitivity of the DNA. This, effect, which was not observed with DNA irradiated under fluid aqueous conditions, would appear to be due to two components; a physical component, and a chemical component which is dependent on the anions used. Addition of alkali metal halides appears to increase the volume of the hydrating layer of water which is formed around the DNA when it is frozen. This appears to increase the target volume when it is irradiated, with an observed increase in damage caused by H2O-+ and non-hydrated electrons from the ionisation of the hydration water. The chemical component, which may be a protective or a sensitising effect, is dependent on the anion in the system. The scavenging of electrons produced from the direct action of gamma radiation on DNA has been demonstrated using the intercalator, mitozantrone. This was demonstrated using plasmid DNA irradiated under frozen aqueous solutions, and compared with the e.s.r. spectroscopy results obtained by my coworkers. Finally, the protection of DNA by free-thiols has been investigated. Under indirect, dilute aqueous conditions, the amount of protection to plasmid DNA was observed to increase with increasing positive charge on the thiols. Under direct, frozen aqueous conditions, the radiosensitivity of plasmid DNA by the compounds used was less clear cut. Possible reasons for this contrast are discussed. The effect of a novel aminothiol with a +3 positive charge on the amount of damage to tissue culture cells was also investigated.
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Bücher zum Thema "DNA Effect of radiation on"

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NATO Advanced Research Workshop on the Early Effects of Radiation on DNA (1990 San Miniato, Italy). The early effects of radiation on DNA. Berlin: Springer-Verlag, 1991.

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NATO Advanced Study Institute on Radiation Carcinogenesis and DNA Alterations (1984 Kerkyra, Greece). Radiation carcinogenesis and DNA alterations. New York: Plenum Press, 1986.

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Braddock, Martin. Effects of radiation on DNA. Salford: University of Salford, 1985.

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4

Przybytniak, Grażyna. Rodniki powstające w DNA i jego nukleotydach pod wpływem promieniowania jonizującego. Warszawa: Instytut Chemii i Techniki Jądrowej, 2004.

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Vilenchik, M. M. Nestabilʹnostʹ DNK i otdalennye vozdeĭstvii͡a︡ izlucheniĭ. Moskva: Ėnergoatomizdat, 1987.

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Marikki, Laiho, und SpringerLink (Online service), Hrsg. Molecular Determinants of Radiation Response. New York, NY: Springer Science+Business Media, LLC, 2011.

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Fielden, E. M., und P. O’Neill, Hrsg. The Early Effects of Radiation on DNA. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75148-6.

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Sharpatyĭ, V. A. Radiat︠s︡ionnai︠a︡ khimii︠a︡ biopolimerov. Moskva: GEOS, 2008.

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UCLA SymposiaColloquium, Ionizing Radiation Damage to DNA, Molecular Aspects (1990 Lake Tahoe, Calif.). Ionizing radiation damage to DNA: Molecular aspects : proceedings of a Radiation Research Society-UCLA Symposia Colloquium held at Lake Tahoe, California, January 16-21, 1990. Herausgegeben von Wallace Susan S, Painter Robert B, Radiation Research Society (U.S.) und University of California, Los Angeles. New York, N.Y: Wiley-Liss, 1990.

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Kruszewski, Marcin. Podłoże odwrotnej krzyżowej oporności komórek L5178Y na promieniowanie jonizujące i nadtlenek wodoru. Warszawa: Instytut Chemii i Techniki Jądrowej, 1999., 1999.

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Buchteile zum Thema "DNA Effect of radiation on"

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Kiefer, Jürgen. „Photo- and Radiation Chemistry of DNA“. In Biological Radiation Effects, 104–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83769-2_6.

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Sagstuen, E., E. O. Hole, W. H. Nelson und D. M. Close. „The Effect of Environment upon DNA Free Radicals“. In The Early Effects of Radiation on DNA, 215–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75148-6_23.

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Swenberg, Charles E. „DNA and Radioprotection“. In Terrestrial Space Radiation and Its Biological Effects, 675–95. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1567-4_47.

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Barendsen, G. W. „The Dependence of Dose-Effect Relations for Various Responses in Mammalian Cells on Radiation Quality, Implications for Mechanisms of Carcinogenesis“. In Radiation Carcinogenesis and DNA Alterations, 583–91. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5269-3_49.

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Edwards, A. A., und D. C. Lloyd. „Chromosomal Damage in Human Lymphocytes: Effect of Radiation Quality“. In The Early Effects of Radiation on DNA, 385–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75148-6_40.

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van der Schans, G. P. „Effect of Dose Modifiers on Radiation-Induced Cellular DNA Damage“. In The Early Effects of Radiation on DNA, 347–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75148-6_36.

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Frankenberg, D. „Repair of DNA Damage and its Effect on RBE - An Experimental Approach“. In The Early Effects of Radiation on DNA, 287–305. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75148-6_30.

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McClellan, R. O., B. B. Boecker, F. F. Hahn, B. A. Muggenburg und R. G. Cuddihy. „Carcinogenic Effects of Inhaled Radionuclides“. In Radiation Carcinogenesis and DNA Alterations, 147–54. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5269-3_8.

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Field, S. B. „Non-Stochastic Effects: Compatibility with Present ICRP Recommendations“. In Radiation Carcinogenesis and DNA Alterations, 539–57. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5269-3_45.

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Olive, P. L. „Discussion: Cellular DNA Strand Breakage“. In The Early Effects of Radiation on DNA, 107–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75148-6_11.

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Konferenzberichte zum Thema "DNA Effect of radiation on"

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Ram, Vineetha, VISHNU KAVUNGAL, Pradeep Chandran und Nampoori Vadakkedathu Parameswaran Narayana. „Silver Nanoparticles as Radiation Absorbers to Reduce the Effect of Mobile Phone Radiation on DNA“. In International Conference on Fibre Optics and Photonics. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/photonics.2012.w3b.3.

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Prahardi, R., und Arundito Widikusumo. „Zero Dose“. In Seminar Si-INTAN. Badan Pengawas Tenaga Nuklir, 2021. http://dx.doi.org/10.53862/ssi.v1.062021.008.

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Ionizing radiation in the medical world has long been used, both for diagnostic and therapeutic purposes. But the use of ionizing radiation, besides helping a lot in diagnosis and therapy, ionizing radiation is also hazardous for us. The effects of ionizing radiation on humans are divided into two types, namely stochastic effects, and non-stochastic (deterministic) effects. Of the two kinds of effects caused by ionizing radiation, the stochastic effect needs special attention. Because the dose-limiting parameter does not exist, how much radiation dose can cause the stochastic effect. We only have the principle that no matter how small the radiation that hits us, it will still impact us. The mechanism for this effect is either a direct effect or an indirect effect, or a newly discovered effect, namely the bystander effect, all of which lead to DNA damage. This DNA damage will cause various kinds of health problems for us. Keywords: Stochastic Effect, DNA Damage. Gene Mutation, Bystander Effect
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Prahardi, R., und Arundito Widikusumo. „Pentingnya Pendidikan dan Pelatihan Bagi Pekerja Radiasi“. In Seminar Si-INTAN. Badan Pengawas Tenaga Nuklir, 2021. http://dx.doi.org/10.53862/ssi.v1.062021.005.

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Ionizing radiation, when it hits our bodies, can ionize and excite the atomic nuclei of cells. Ionization and excitation will cause DNA damage either directly or indirectly. DNA damage is direct if ionizing radiation hits DNA, while DNA damage is indirectly through the formation of free radicals (atoms with unpaired electrons) and has a very damaging effect on DNA. Therefore, safety in ionizing radiation, including its use in the medical world, is essential. Protection includes safety avoiding deterministic effects and stochastic effects. To protect against both deterministic and stochastic effects, the role of the radiographer is significant. Heinrich (1980) estimates that (85%) accidents are the result of the contribution of unsafe work behavior (unsafe act). Radiation accidents reported by the United States Energy Atomic Commission from 1960-1968 were caused by operator error (68%), procedural errors (8%), equipment damage (15%), and others (9%). When viewed in detail, the operator's errors were not conducting a radiation survey (46%), not following procedures (36%), not using protective equipment (6%), human error (6%), and calculating radiation exposure errors (6%). Therefore, the radiographer must know and understand ionizing radiation, its dangers, and the application of radiation protection from the results of a survey conducted at Prof. Hospital. Dr. Margono Soekarjo Purwokerto to 22 radiographers showed that the level of understanding of ionizing radiation, the dangers, and the application of radiation protection is still low. Therefore education and training are very much needed for them. Keywords: Radiation Hazard, Radiation Protection, Radiographer Education and Training
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Dicu, Tiberius, Ion D. Postescu, Vasile Foriş, Ioana Brie, Eva Fischer-Fodor, Valentin Cernea, Mircea Moldovan, Constantin Cosma, Madalin Bunoiu und Iosif Malaescu. „The Effect of a Grape Seed Extract on Radiation-Induced DNA Damage in Human Lymphocytes“. In PROCEEDINGS OF THE PHYSICS CONFERENCE: TIM—08. AIP, 2009. http://dx.doi.org/10.1063/1.3153444.

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Cao, En-Hua, Ju-jun Wang und Shu-min Xin. „Nonlinear biological effects of high-intensity visible laser radiation on DNA“. In OE/LASE'93: Optics, Electro-Optics, & Laser Applications in Science& Engineering, herausgegeben von Steven L. Jacques und Abraham Katzir. SPIE, 1993. http://dx.doi.org/10.1117/12.147670.

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Bera, Partha P., Henry F. Schaefer, George Maroulis und Theodore E. Simos. „Elementary Energetic Effects of Radiation Damage to DNA and RNA Subunits“. In Computational Methods in Science and Engineering. AIP, 2007. http://dx.doi.org/10.1063/1.2826997.

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Janic, Branislava, Fangchao Liu, Kevin Bobbitt, Stephen Brown, Guangzhao Mao, Indrin J. Chetty, Benjamin Movsas und Ning Winston Wen. „Abstract 1376: Effect of gold nanoparticle on radiation induced DNA damage in MCF7 breast cancer cells“. 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.am2018-1376.

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Dan, Tu, Ajay Palagani, Tiziana DeAngelis, Sunny Han, Lance Liotta, Richard Pestell und Nicole Simone. „Abstract 3064: MicroRNA-21 enhances the effect of ionizing radiation via alteration of the DNA damage response“. In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3064.

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Vasilyeva, Irina, O. Korytov, V. Bespalov, A. Semenov, G. Tochil'nikov, S. Ivanov und L. Korytova. „EFFECTS OF RADIATION EXPOSURE OF THE BLADDER ON EARLY CHANGES OF EXTRACELLULAR DNA AND OTHER INDICATORS OF PERIPHERAL BLOOD“. In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9b37c7f8.86673968.

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On the model of radiation cystitis in rats, a decrease in the number of blood cells was found 6 h after local irradiation and an increase in extracellular DNA level was found in 6-24 h with normalization 48 h after exposure. The relative change in the content of extracellular DNA (0 h against 6 h) correlated with changes in triglycerides (0 h against 24 h).
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Vishnu, K., B. Nithyaja, M. Kailasnath und V. P. N. Nampoori. „Studies on Thermal Effects of Mobile Phone Radiation on DNA by Thermal Lens Technique“. In International Conference on Fibre Optics and Photonics. Washington, D.C.: OSA, 2012. http://dx.doi.org/10.1364/photonics.2012.mpo.5.

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Berichte der Organisationen zum Thema "DNA Effect of radiation on"

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Hosselet, S. The effect of radiation penetration on DNA single-strand breaks in rat skin explants. Office of Scientific and Technical Information (OSTI), Januar 1989. http://dx.doi.org/10.2172/5561134.

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Peak, J. G., T. Ito, M. J. Peak und F. T. Robb. DNA damage produced by exposure of supercoiled plasmid DNA to high- and low-LET ionizing radiation: Effects of hydroxyl radical quenchers. DNA breakage, neutrons, OH radicals. Office of Scientific and Technical Information (OSTI), August 1994. http://dx.doi.org/10.2172/10172487.

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Sevilla, M. D. Mechanisms for radiation damage in DNA. Office of Scientific and Technical Information (OSTI), Dezember 1992. http://dx.doi.org/10.2172/7176057.

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Sevilla, M. D. Mechanisms for radiation damage in DNA. Office of Scientific and Technical Information (OSTI), Januar 1990. http://dx.doi.org/10.2172/5018151.

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Sevilla, M. D. Mechanisms for radiation damadge in DNA. Office of Scientific and Technical Information (OSTI), November 1994. http://dx.doi.org/10.2172/87116.

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Wilson, David. Repair Machinery for Radiation-Induced DNA Damage. Fort Belvoir, VA: Defense Technical Information Center, Juli 2001. http://dx.doi.org/10.21236/ada396847.

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Wilson, David. Repair Machinery for Radiation-Induced DNA Damage. Fort Belvoir, VA: Defense Technical Information Center, Juli 2000. http://dx.doi.org/10.21236/ada384080.

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Thompson, Lawrence H. Repair Machinery for Radiation-Induced DNA Damage. Fort Belvoir, VA: Defense Technical Information Center, November 2003. http://dx.doi.org/10.21236/ada423482.

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Osman, R. Molecular mechanisms in radiation damage to DNA. Office of Scientific and Technical Information (OSTI), Oktober 1991. http://dx.doi.org/10.2172/5816640.

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Thompson, Lawrence H. Repair Machinery for Radiation-Induced DNA Damage. Fort Belvoir, VA: Defense Technical Information Center, Juli 2002. http://dx.doi.org/10.21236/ada407373.

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