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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.
Повний текст джерелаАнотація:
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.<br>Medicine, Faculty of<br>Pathology and Laboratory Medicine, Department of<br>Graduate
2
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.
Повний текст джерелаАнотація:
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.<br><p>At the time of doctoral defense, the following paper was unpublished and had a status as follows: Paper 2: Manuscript.</p>
3
Morabito, Brian Joseph. "Quantitating radiation induced DNA breaks by capillary electrophoresis." Thesis, Georgia Institute of Technology, 1997. http://hdl.handle.net/1853/16339.
Повний текст джерела
4
Braddock, M. "Effects of radiation on DNA." Thesis, University of Salford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356177.
Повний текст джерела
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.
Повний текст джерела
6
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.
Повний текст джерела
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.
Повний текст джерелаАнотація:
Thesis (PhD)--Stellenbosch University, 2001.<br>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.<br>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.
8
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.
Повний текст джерела
9
Sweeney, Marion Carol. "The effects of gamma radiation on DNA." Thesis, University of Leicester, 1986. http://hdl.handle.net/2381/33943.
Повний текст джерела
10
Elsy, David. "The effects of gamma-radiation on DNA." Thesis, University of Leicester, 1991. http://hdl.handle.net/2381/33664.
Повний текст джерелаАнотація:
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.
11
Alvarado, Chacón Fresia. "Ion induced radiation damage on the molecular level." [S.l. : Groningen : s.n. ; University Library of Groningen] [Host], 2007. http://irs.ub.rug.nl/ppn/305192396.
Повний текст джерела
12
Camacho, Inês Sofia Cortes Eusébio. "Effects of UV radiation exposure on DNA and DNA repair enzymes." Master's thesis, Faculdade de Ciências e Tecnologia, 2012. http://hdl.handle.net/10362/8263.
Повний текст джерелаАнотація:
Dissertação para obtenção do Grau de Mestre em
Biotecnologia<br>DNA integrity in the cell is under constant threat from damaging agents of endogenous or
exogenous origin, such as UV light, ionizing radiation and oxidative stress. Although the effects of these carcinogens on DNA have been extensively studied, very little is known about their effect on DNA repair enzymes.
The aim of the present work was the study of the effect of UV radiation on E. coli Endonuclease III, a DNA glycosylase belonging to base excision repair system. This enzyme was homologously overexpressed and then purified with a Fe/protein ratio of 3.88 ± 0.63 (fully‐loaded form).
Endonuclease III exposure to UV radiation for 45 min (19.77 kJ dose) may lead to the destruction of the Fe‐S bonds of the [4Fe‐4S] cluster or to the conversion of this center into a different redox state.
Electrophoretic mobility shift assays with protein‐DNA complex showed that Endonuclease III binding to plasmid DNA promotes a retardation of the free supercoiled DNA band, indicative of Endonuclease III‐DNA complex(es) formation. These assays also showed that Endonuclease III is able
to bind both linear and supercoiled plasmid DNA, although with higher affinity for the linear form.
Electrophoretic mobility shift assays performed after 45 min of UV irradiation (19.77 kJ) revealed that although shift occurred, the complexes formed were unstable and dissociated during electrophoresis. Moreover, the presence of aggregates suggests the unfolding of some Endonuclease
III molecules. After 6 h of UV irradiation (158.18 kJ) no complexes are formed, leading to the conclusion that Endonuclease III molecules were irreversibly damaged.
The electrochemical studies were performed by cyclic and differential pulse voltammetry
techniques, at room temperature and anaerobic conditions; Endonuclease III and Endonuclease IIIDNA complex were adsorbed on a bare pyrolytic graphite electrode. For the first time, the direct electrochemical response of Endonuclease III unbound to DNA was observed, with a quasi‐reversible
redox couple displaying a midpoint potential of 178 ± 9 mV vs. NHE. Endonuclease III binding to plasmid DNA promotes a positive shift (19 mV vs. NHE) in the characteristic redox couple of Endo III.
Protein‐DNA complex UV irradiation promotes a negative shift in its redox potential of 25 mV vs. NHE.
13
Kabilan, Usha. "Studying the Effect of Low Doses of Ionization Radiation on Senescence in Human Lung Fibroblasts." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40982.
Повний текст джерелаАнотація:
The exposure to high doses of ionizing radiation (>5Gy) is unequivocally associated with increased cancer risk. However, there is substantial experimental evidence showing that in response to low doses of ionizing radiation (LDR: <100mGy), cells and organisms are benefitted with delayed ageing, improved immunity and reduced cancer growth. These intriguing findings have proposed the “Radiation Hormesis” hypothesis. Herein, I studied the senescence effects of LDR exposure to normal human HFL1 cells and examined transcriptional changes. I found that HFL1 cells exposed to 10 mGy of gamma radiation had delayed senescence measured at 12 weeks post-irradiation compared to unirradiated cells. Through qPCR array analysis, I found that genes involved in human cellular senescence functions are differentially regulated in 10 mGy exposed cells at 12 weeks compared to 1-week post-exposure. A nucleolar protein, SIRT7, that belongs to the family of proteins called Sirtuins with known roles in aging, was found to be upregulated transcriptionally in LDR-exposed HFL1 cells. Knocking out SIRT7 protein significantly accelerated senescence in HFL1 cells suggesting a direct role of SIRT7 in the deceleration of senescence and potentially in mediating radiation hormesis. Furthermore, overexpression of the HRAS oncogene strongly accelerated senescence in HFL1 cells through gene expression of cell cycle regulators and checkpoint proteins. Together, my studies revealed that LDR induces unique transcriptional changes resulting in a potentially radio adaptive protective cellular response. I also discuss the HRAS overexpression system as a time-efficient cellular model that could be used to more rapidly study the effect of LDR on senescence using primary cultures.
14
Bykov, Vladimir J. "UV-induced DNA damage in humans /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3345-6/.
Повний текст джерела
15
Malone, Mark E. "The effect of ionising radiation on DNA and its constituents : an EPR study." Thesis, University of Leicester, 1993. http://hdl.handle.net/2381/33797.
Повний текст джерелаАнотація:
This thesis was concerned with the effects of ?-radiation and UV-photoionisation on DNA an its constituents at 77 K. In particular, the work has concentrated on the radical-anion and radical-cation centres, with a view to obtaining a better understanding of the so-called direct mechanism of radiation damage. The ?-irradiation of DNA and its constituents in aqueous LiCl glasses suppresses radical cation formation and gives rise to well resolved radical anion spectra which can be readily studied by EPR spectroscopy. The nucleotides of adenine, cytosine, guanine and cytosine all yield base centred ?-radical anions, which are thought to undergo reversible deprotonation to form neutrally charged radicals. Electron competition studies in DNA, duplex polynucleotides, dinucleotides, and mononucleotide mixtures indicate that the electron affinities of the four bases are of the order C > T >> A ? G. However, the DNA radical anion (DNA. ), has a well resolved doublet spectrum which is indistinguishable from those of T.- and C.- in duplex systems. Consequently it is difficult to judge the proportions of C.- and T.- in these glasses. An alternative method to evaluate the proportions of C.- and T.- in irradiated DNA involves the annealing of frozen aqueous DNA in order to convert the T.- centres into TH. radicals, in which a hydrogen atom is added at C6. These results imply that ca 36 % of the radical anion centres in frozen aqueous DNA are due to T.- centres. The addition of LiCl, NaCl, LiBr and NaClO4 salts to DNA, cause a large increase in the yields of DNA radicals (mainly due to DNA.- centres). However, despite the increase in the radical yields, very little change in the yields of strand breaks are induced by these salts. The results are discussed in terms of an increase in the effective target volume and the reactivities of the salt radicals Cl2.-, Br.- and O.-. Perchlorate glasses and frozen aqueous matrices were employed to investigate the photoionisation of DNA and its constituents at 77 K. The perchlorate glasses scavenge the photoejected electrons and enables the isolation of the organic electron loss centres. In this manner, a number of electron loss radicals were identified. Thymine and cytosine yield N1 deprotonated ?-radical cations with spin centred at C5 and Nl. The radical cations of Nl substituted thymine derivatives (e.g. thymidine), deprotonate at the C5 methyl group to form the TCH2. radical. The nucleosides and nucleotides of cytosine give rise to sugar radicals which are thought to arise from single or multistep hydrogen shifts. A tentative assignment of these radicals has been made. The nucleotides of adenine and guanine give rise to well characterised ?-radical cations which are reversibly deprotonated at the exocyclic amino groups. Photoionisation of mononucleotides mixtures, dinucleotides and DNA indicate that the ease of photoionisation has the order C < T < A << G, and that guanine is the predominant electron loss centre in DNA. These results are discussed in terms of photophysical factors such as excited state lifetimes and ?isc, as well as energy and hole transfer.
16
Allman, Amy Jane. "Effects of UV radiation on Marfan syndrome cells in culture." Virtual Press, 1993. http://liblink.bsu.edu/uhtbin/catkey/879841.
Повний текст джерелаАнотація:
Ultraviolet radiation causes an alteration in DNA by modifying neighboring thymine bases resulting in the formation of a dimer. These dimers block the processes of transcription and translation and ultimately no protein is synthesized and the cell dies. However, DNA repair mechanisms correct this damage by excising the dimer from the DNA strand and inserting replacement bases which are joined to the original strand by DNA ligase. This allows transcription to resume and ultimately protein synthesis to take place.This research focused on determining the DNA damage and subsequent repair levels in a connective tissue disorder, namely Marfan syndrome. This information is important in understanding the clinical expression and management of life threatening conditions in Marfan syndrome individuals.Preliminary results indicate that at 20-25J/m2 UV dose (254nm) Marfan syndrome skin cells show a mean reduced survival value of 12% compared to normal human skin cells. Gel electrophoresis indicates a reduced DNA repair level 24h post UV irradiation for Marfan syndrome skin cells compared to normal human skin cells. These results suggest Marfan syndrome skin cells have reduced survival and DNA repair levels compared to normal human skin cells.<br>Department of Biology
17
Fulford, Jonathan. "Quantification of complex DNA damage by ionising radiation : an experimental and theoretical approach." Thesis, Brunel University, 2000. http://bura.brunel.ac.uk/handle/2438/5782.
Повний текст джерелаАнотація:
Ionising radiation potentially produces a broad spectrum of damage in DNA including single and double strand breaks (ssb and dsb) and base damages. It has been hypothesised that sites of complex damage within cellular DNA have particular biological significance due to an associated decreased efficiency in repair. The aim of this study is to gain further understanding of the formation of complex DNA damage. Irradiations of plasmid DNA illustrate that an increase in ionising density of the radiation results in a decrease in ssb yields/Gy but an increase in dsb per ssb, indicative of an increase in the number of complex damage sites per simple isolated damage site. As the mechanism for damage formation shifts from purely indirect at low scavenging capacities to a significant proportion of direct at higher scavenging capacities the proportion of complex damage increases. Comparisons with the yields of ssb and dsb simulated by Monte-Carlo calculations for AIK USX and a-particles also indicate this correspondence. The ionisation density of low energy, secondary electrons produced by photons was assessed experimentally from the dependence of the yield of OH radicals escaping intra-track recombination on photon energy. As energy decreases the OH radical yield initially decreases reflecting an increased ionisation density. However, with further decrease in photon energy the yield of OH radicals increases in line with theoretical calculations. Base damage yields were determined for low and high ionising density radiation over a range of scavenging capacities. As scavenging capacity increases the base damage:ssb ratios increases implying a contribution from electrons to base damage. It is proposed that base damage contributes to DNA damage complexity. Complex damage analysis reveals that at cell mimetic scavenging capacities, 23% and 72% of ssb have an additional spatially close damage site following y-ray and a-particle irradiation respectively.
18
Ladin, Loren Guerrero 1959. "Effect of ultraviolet light on reproduction in Hydra littoralis." Thesis, The University of Arizona, 1989. http://hdl.handle.net/10150/277085.
Повний текст джерелаАнотація:
The "DNA Damage Hypothesis" pertaining to the evolution of sex was tested using Hydra littoralis. DNA damage was produced by irradiating whole live hydra with ultraviolet light. A curve of uv light dosage vs. survival was constructed. Estimations of threshold fluence and LD50 were made from the survival curve. In four separate experiments, using various combinations of environmental temperatures, uv doses, and number of doses, frequencies of asexual and sexual reproduction were observed and compared. The hydra that received uv treatments did not show an increase in the consequent amount of sexual reproduction, and actually showed a decrease. An increase in the amount of sexual reproduction following DNA damage is predicted by the DNA damage hypothesis, therefore these results do not support this theory. The data was also used to make contradictory observations regarding the "stress hypothesis" for the occurrence of sexual reproduction in hydra.
19
Baker, Mike, and University of Lethbridge Faculty of Arts and Science. "Role of epigenetic changes in direct and indirect radiation effects." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2008, 2008. http://hdl.handle.net/10133/650.
Повний текст джерелаАнотація:
For over 100 years, cancer radiation therapy has provided patients with increased
survival rates. Despite this success, radiation exposure poses a threat to the progeny of
exposed parents. It causes transgenerational genome instability that is linked to
transgenerational carcinogenesis. The exact mechanisms in which this instability occurs
have yet to be discovered. Current evidence points to their epigenetic nature, specifically
changes in DNA methylation.
Using mouse and rat models, this thesis investigated the transgenerational effects
of radiation in the offspring from parents who received whole body or localized exposure
to ionizing radiation (IR). Both types of exposure resulted in significant global DNA
hypomethylation in the somatic tissues of the progeny. These changes were paralleled by
the significantly decreased levels of methyltransferases and methyl-CpG-binding protein.
In summary, our results suggest that both localized and whole body parental
exposures to IR result in transgenerational epigenetic instability within the unexposed
offspring.<br>vii, 106 leaves : ill. ; 29 cm.
20
Tamminga, Jan, and University of Lethbridge Faculty of Arts and Science. "Radiation-induced epigenome deregulation in the male germline." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2008, 2008. http://hdl.handle.net/10133/746.
Повний текст джерелаАнотація:
Approximately 45% of men will develop cancer during their lifetime; some of which will be of reproductive age (Canadian Cancer Society, 2008). Current advances in treatment regimens such as radiotherapy have significantly lowered cancer-related mortality rates; however, one major quality-of-life issue in cancer survivors is the ability to produce healthy offspring. Exposure to ionizing radiation (IR) leads to genomic instability in the germline, and further to transgeneration genome instability in unexposed offspring of preconceptionally exposed parents. The results presented in this thesis define, in part, the molecular consequences of direct and indirect irradiation for the male germline. Direct exposure results in a significant accumulation of DNA damage, altered levels of global DNA methylation and microRNAome dysregulation of testis tissue. Localized cranial irradiation results in a significant accumulation of unrepaired DNA lesions and loss of global DNA methylation in the rodent (rat) germline. Biological consequences of the changes observed are discussed.<br>xii, 121 leaves : ill. ; 29 cm.
21
VALGODE, FLAVIA G. S. "Avaliação do dano radioinduzido, capacidade de reparo e morte celular em células humanas tumorais (T-47D e MCF-7) e nao tumorais (MCF-10) de mama." reponame:Repositório Institucional do IPEN, 2008. http://repositorio.ipen.br:8080/xmlui/handle/123456789/11710.
Повний текст джерелаАнотація:
Made available in DSpace on 2014-10-09T12:54:58Z (GMT). No. of bitstreams: 0<br>Made available in DSpace on 2014-10-09T14:07:14Z (GMT). No. of bitstreams: 0<br>Dissertacao (Mestrado)<br>IPEN/D<br>Instituto de Pesquisas Energeticas e Nucleares - IPEN/CNEN-SP
22
Gonon, Géraldine. "Space radiation-induced bystander effect : kinetics of biologic responses, mechanisms, and significance of secondary radiations." Phd thesis, Université de Franche-Comté, 2011. http://tel.archives-ouvertes.fr/tel-00987717.
Повний текст джерелаАнотація:
Widespread evidence indicates that exposure of cell cultures to α particles results in significant biological changes in both the irradiated and non-irradiated bystander cells in the population. The induction of non-targeted biological responses in cell cultures exposed to low fluences of high charge (Z) and high energy (E) particles is relevant to estimates of the health risks of space radiation and to radiotherapy. Here, we investigated the mechanisms underlying the induction of stressful effects in confluent normal human fibroblast cultures exposed to low fluences of 1000 MeV/u iron ions (linear energy transfer (LET) ~151 keV/µm), 600 MeV/u silicon ions (LET ~50 keV/µm) or 290 MeV/u carbon ions (LET ~13 keV/µm). We compared the results with those obtained in cell cultures exposed, in parallel, to low fluences of 0.92 MeV/u α particles (LET ~109 keV/µm).Induction of DNA damage, changes in gene expression, protein carbonylation and lipid peroxidation during 24 h after exposure of confluent cultures to mean doses as low as 0.2 cGy of iron or silicon ions strongly supported the propagation of stressful effects from irradiated to bystander cells. At a mean dose of 0.2 cGy, only ~1 and 3 % of the cells would be targeted through the nucleus by an iron or silicon ion, respectively. Within 24 h post-irradiation, immunoblot analyses revealed significant increases in the levels of phospho-TP53 (serine 15), p21Waf1 (also known as CDKN1A), HDM2, phospho-ERK1/2, protein carbonylation and lipid peroxidation. The magnitude of the responses suggested participation of non-targeted cells in the response. Furthermore, when the irradiated cell populations were subcultured in fresh medium shortly after irradiation, greater than expected increases in the levels of these markers were also observed during 24 h. Together, the results imply a rapidly propagated and persistent bystander effect. In situ analyses in confluent cultures showed 53BP1 foci formation, a marker of DNA damage, in more cells than expected based on the fraction of cells traversed through the nucleus by an iron or silicon ion. The effect was expressed as early as 15 min after exposure, peaked at 1 h and decreased by 24 h. A similar tendency occurred after exposure to a mean absorbed dose of 0.2 cGy of 3.7 MeV α particles, but not after 0.2 cGy of 290 MeV/u carbon ions.Analyses in dishes that incorporate a CR-39 solid state nuclear track detector bottom identified the cells irradiated with iron or silicon ions and further supported the participation of bystander cells in the stress response. Mechanistic studies indicated that gap junction intercellular communication, DNA repair, and oxidative metabolism participate in the propagation of the induced effects.We also considered the possible contribution of secondary particles produced along the primary particle tracks to the biological responses. Simulations with the FLUKA multi-particle transport code revealed that fragmentation products, other than electrons, in cells cultures exposed to HZE particles comprise <1 % of the absorbed dose. Further, the radial spread of dose due to secondary heavy ion fragments is confined to approximately 10-20 µm Thus, the latter are unlikely to significantly contribute to the stressful effects in cells not targeted by primary HZE particles.
23
Logan, Ian D. "The effect of low intensity laser irradiation and low level, low LET ionising radiation on DNA within mammalian cells." Thesis, University of Ulster, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338280.
Повний текст джерела
24
Boon, P. J. "ESR studies on the effects of ionizing radiation on DNA plus additives." Thesis, University of Leicester, 1985. http://hdl.handle.net/2381/34020.
Повний текст джерелаАнотація:
In this study the direct effect of ionising radiation on DNA plus additives has been studied using both ESR spectroscopy and plasmid DMA (for strand break analysis). The primary radicals were identified as the thymine radical-anion, T', and guanine radical-cation, G'*'. Under normal conditions these were formed in approximately equal yields as defined by careful computer simulations. Certain additives such as oxygen, nitroimidazoles, silver ions and the rest of the nuclear complement (i.e. RNA and histone proteins) , were added to study their effects on the relative yields of T" and G". In all cases, they were shown to capture electrons in competition with T" and have little or no effect on the yield of G"*". In the case of oxygen and nitroimidazoles the effect of reducing the yield of T" radicals was looked at using strand break analyses. Essentially this was found to protect the DNA. Since both single and double strand breaks were found at significant levels when G+ and T~ were the only detectable initial radicals, one must conclude that these radicals are responsible for strand breaks. Fran the relatively high number of double strand breaks found, we deduce that G'*' and T" centres must be close togetlier (in a range of ca. 10-50 A), and that both may give rise to strand breaks, by as yet undefined pathways. In a separate study (Chapter 4), the reaction between superoxide ions, O2"/ and dimethyl formamide has been investigated by ESR spectroscopy. Strong evidence in favour of addition of O2" at the C=0 group to give a relatively stable peroxy radical intermediate has been obtained. This has implications for the mechanism of action of O2" formed both as a result of radiation damage and by other means. Appendix I describes a study of various simple aldehyde and ketone radical-cations, using ESR spectroscopy. Interpretations of these spectra are given, together with structural implications. Appendix II is a paper on work carried out on the ESR spectra of hydroxyl radicals in aqueous glasses. This work was done in collaboration with H. Riederer and J. Hiittermann.
25
Koturbash, Igor, and University of Lethbridge Faculty of Arts and Science. "Molecular mechanisms of radiation-induced bystander effects in vivo." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2008, 2008. http://hdl.handle.net/10133/664.
Повний текст джерелаАнотація:
Ionizing radiation (IR), along with being an important diagnostic and treatment
modality, is a potent tumor-causing agent, and the risk of secondary radiation
treatment-related cancers is a growing clinical problem. Now some studies propose to
link secondary radiation-induced cancers to an enigmatic phenomenon of bystander
effects, whereby the exposed cells send signal damage and distress to their naïve
neighbors and result in genome destabilization and carcinogenesis. Yet, no data
existed on the bystander effects in an organ other than an exposed one. With this in
mind, we focused on the analysis of existence and mechanisms of radiation-induced
bystander effects in vivo. We have found that bystander effects occur in vivo in
distant skin and spleen following half-body or cranial irradiation. These bystander
effects resulted in elevated DNA damage, profound dysregulation of epigenetic
machinery, and pronounced alterations in apoptosis, proliferation and gene
expression. Bystander effects also exhibited persistency and sex specificity. The
results obtained while using the animal model systems can potentially be extrapolated
to different animals and humans.<br>xiii, 208 leaves : ill. ; 29 cm.
26
Carpenter, Lucy. "DNA repair pathways involved in determining the level of cytotoxicity of environmentally relevant UV radiation." Thesis, Lancaster University, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340566.
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Jones, George Donal Dransfield. "The direct effects of ionizing radiation on DNA and its higher ordered structures." Thesis, University of Leicester, 1987. http://hdl.handle.net/2381/9691.
Повний текст джерелаАнотація:
This thesis investigates the effects of ionizing radiation on frozen aqueous solutions of DNA using e.s.r. spectroscopy and a plasmid (pBR322) strand break assay. To elucidate the mechanisms subsequent to primary ionic radical formation (G˙+ and T˙¯), additives that influence the radiolytic processes were included prior to irradiation. The presence of hydrogen peroxide (Chapter Three) switched the mechanism from direct damage to a pathway in part mediated through oxygen centred radicals (˙OH, HO˙2) and resulted in a modest increase in the number of strand breaks (i.e. radiosensitization). E.s.r. observations showed the appearance of sugar radicals (strand break precursors) which were lost at temperatures well below those of base radicals. The inclusion of a variety of thiols (Chapter Four) resulted in no change to either G˙ + or T˙¯, However, on warming, the normal pattern of radical reactions was dramatically modified, the DNA radical centres being abruptly reduced in concentration. In anoxia this was concomitant with the appearance of RSSR ¯, and strand breaks were noted to decrease (i,e. radioprotection). Under oxic conditions the degree of repair was a function of the relative concentration of oxygen and thiol. E.s.r. indicated repair of DNA centred peroxyl radicals and also RSO˙2 formation. The latter may react with DNA and account for attenuation, by oxygen, of protection afforded by thiols at low concentrations. The effects of ionizing radiation on higher ordered DNA structures (nucleohistone, chromatin and cell nuclei) has been investigated (Chapter Five). Relative to DNA, all systems gave equivalent yields of G˙+, together with protein electron-loss centres (Hist)˙+. However, T˙¯ yields were enhanced, the increase being greatest for nuclei. For the protein component it was suggested that (Hist)˙+ are amide cations, readily trapped by loss of N-H protons, but that the electrons are Mobile and able to transfer to DNA. Mechanisms leading to strand breaks, involving intramolecular hydrogen atom abstraction by directly induced base radicals from neighbouring sugar residues, are proposed (Appendix B) and compared with those obtained for hydroxyl radical damage.
28
McClymont, John Douglas. "ESR studies of the effects of complexing agents on radiation damage in DNA." Thesis, University of Leicester, 1990. http://hdl.handle.net/2381/33802.
Повний текст джерелаАнотація:
The effects of a range of complexing agents on the radiation damage routes in frozen aqueous DNA have been analyzed by ESR techniques in a semi-quantitative way. Establishment of additive-free DNA standards for this study revealed an ESR pattern different from the four elementary shapes which contributed ∼ 13X of the total spin seen after annealing to 210 K. It is proposed that this represents a population of sugar radicals; hitherto unseen intermediates in additive-free systems between secondary base radicals and strand breaks. The intercalating aminoanthraquinones, mitoxantrone and ametantrone, were found to compete very efficiently with thymine for electron capture, and behaved as protecting agents. Concomitant strand break studies did not support this, and more extensive ESR studies suggested that the intercalator radical centre could also lead to strand breaks. It is therefore proposed that the mode of action of these drugs does not involve free radical processes in DNA. Use of these agents provided evidence that electron migra tion in DNA is much more extensive than previously thought. Copper ions were found to reduce the amounts of T/TH detected, with no effect on G . During this evaluation, evidence appeared for the existence of a site on DNA that could bind two Cu(II) ions so close together that they became ESR silent. Of special interest was the finding that this binding was preferred over that of single Cu(II) ions, and it is proposed that this might have a physiological significance. The dominance of thymine over cytosine as the site of electron capture is reinforced by the above studies, but it is suggested that it is the nature of the system under study that determines the ratio of T to C.
29
Valente, Marco. "Signalling detection of DNA damage induced by low doses of ionizing radiation in human lymphocytes." Versailles-St Quentin en Yvelines, 2011. http://www.theses.fr/2011VERS0021.
Повний текст джерелаАнотація:
Etude du lien entre radiosensibilité clinique d’un patient et de ses lymphocytes irradiés in vitro dans le but de faire un test prédictif de la radiosensibilité individuelle. La radiosensibilité clinique est quantifiée par les effets secondaires d’une radiothérapie et la sensibilité cellulaire est mesurée grâce à la cinétique d’apparition/disparition des doubles cassures de l’ADN radio-induites (marquées par des foyers gamma-H2AX). Pour rendre ce protocole utilisable en application clinique, on a amélioré la viabilité de l'échantillon et augmenté la vitesse d’analyse. Enfin, nous nous sommes concentrés sur la réponse à des faibles doses dans un autre contexte: la réponse radio-adaptative. Elle est caractérisée par une réponse cellulaire, à une forte dose d’exposition, moins importante lorsqu’elle est précédée par l’exposition à une faible dose. Ce type de réponse a été observé pour le taux de translocations dans les lymphocytes CD4-positifs mais pas pour la signalisation gamma-H2AX<br>Study of the relationship between the clinical radiosensitivity of a patient and his lymphocytes irradiated in vitro in order to establish a predictive test of individual radiosensitivity. Clinical radiosensitivity was quantified by the intensity of radiotherapy side effects and cellular sensitivity was measured by the kinetics of appearance/disappearance of radiation-induced DNA double-strand breaks (marked by gamma-H2AX foci). To make the protocol viable for clinical application, sample viability and analysis speed were improved. Finally, we focused on low-dose response in another context: radio-adaptive response. This phenomenon is characterized by a weaker cellular response to a high dose exposure when it is preceded by a low-dose exposure. This type of response was observed for the two-way translocation rate in CD4-positive lymphocytes but not for gamma-H2AX signaling
30
Jones, Matthew Dunford. "Effects of radiation on the Gâ†2/M checkpoint in human tumour cells of differing radiosensitivities." Thesis, University of Liverpool, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387452.
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AQUINO, SIMONE. "Efeitos da radiacao gama no crescimento de Aspergillus flavus produtor de aflatoxinas e no emprego da tecnica da Reacao em Cadeia da Polimerase (PCR) em amostras de graos de milho inoculadas artificialmente." reponame:Repositório Institucional do IPEN, 2003. http://repositorio.ipen.br:8080/xmlui/handle/123456789/11253.
Повний текст джерелаАнотація:
Made available in DSpace on 2014-10-09T12:49:58Z (GMT). No. of bitstreams: 0<br>Made available in DSpace on 2014-10-09T14:02:55Z (GMT). No. of bitstreams: 0<br>Dissertacao (Mestrado)<br>IPEN/D<br>Instituto de Pesquisas Energeticas e Nucleares - IPEN/CNEN-SP
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McRae, Dorothy A., and University of Lethbridge Faculty of Arts and Science. "Radiation induced epigenetic dysregulation in rat mammary gland tissue / Dorothy A. McRae." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Biological Sciences, c2010, 2010. http://hdl.handle.net/10133/2615.
Повний текст джерелаАнотація:
Most breast cancer patients undergo radiation diagnostics and are also treated with radiotherapy. In addition to being an important treatment modality, ionizing radiation (IR) is a potent tumour-causing agent that has been linked to breast cancer development. However, the exact molecular etiology of IR-induced mammary gland carcinogenesis remains unknown.
We set out to analyze the role of DNA methylation in mammary gland responses to low dose IR using a well-established rat model. We also studied low dose IR effects on global gene expression and microRNAome. We found that exposure to low, mammography-like dose of IR led to a significant loss of global DNA methylation in rat mammary gland tissue. Furthermore, low dose IR significantly affected rat mammary gland transcriptome and microRNAome.
The datasets generated within the scope of this thesis may be used to identify novel predictive biomarkers for assessment of the magnitude of IR effects on mammary gland tissue.<br>xi, 120 leaves ; 29 cm
33
Curwen, Gillian B. "G₂ chromosomal radiosensitivity in childhood and adolescent cancer survivors and their offspring." Thesis, St Andrews, 2008. http://hdl.handle.net/10023/425.
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34
Ralph, Emma Louise. "The effects of UV radiation on meiotic DNA replication and Cdt1 stability in fission yeast." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436991.
Повний текст джерела
35
Bellamy, Michael Bruce. "A double strand DNA break model of photon and electron relative biological effectiveness." Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/47711.
Повний текст джерелаАнотація:
The ICRP recommends a radiation weighting factor of one for all low-LET radiation. However, many experimental studies find inconsistencies between low-LET RBE and the ICRP's current radiation weighting factor. Generally, there is evidence that dependence exists between radiation energy and radiation RBE where lower energy radiations tend to have a greater biological effect than higher energy radiation. Specifically, the radiations of tritium and carbon K-shell x-rays have been studied in numerous experiments and the biological effects of both of these radiations are consistently greater than that of Co-60.
In this work, the relationship between radiation energy and radiation effect has been investigated with the use of a newly developed double strand break (DSB) yield estimation algorithm. This algorithm makes use of a detailed solenoidal 30 nm DNA chromatin model to describe the radiation-sensitive biological target. In addition to the DNA model, NOREC, an event by event Monte Carlo code, was used in this algorithm to characterize the electron track. As an alternative to the conventional approach of computationally simulating DNA damage by spatial overlay of an electron track on DNA, this algorithm instead focuses on quantifying the distance between ionizations in an electron track and next determining the likelihood that any given ionization pair forms a DSB. The first step of the algorithm involves electron characterization while the second step relies on DNA molecule characterization. By assuming a DSB biological endpoint and determining the DSB yield as a function of electron energy, energy dependent RBE values were estimated for monoenergetic electrons from 10 eV to 1 MeV.
Photon RBE values, x-ray RBE values and radionuclide RBE values were also calculated and reported in this work in addition to electron RBE values. Photon RBE values were estimated based upon the electron RBE calculation. Photon RBE values were reported from 1 eV to 10 MeV. In turn, x-ray RBE values were calculated based upon photon values for several tube voltage and filter combinations. Finally, RBE values for over 1000 radionuclides were estimated and reported.
36
Aquino, Simone. "Efeitos da radiação gama no crescimento de aspergillus flavus produtor de aflatoxinas e no emprego da técnica da reação em cadeia da polimerase (PCR) em amostras de grãos de milho inoculadas artificialmente." Universidade de São Paulo, 2004. http://www.teses.usp.br/teses/disponiveis/85/85131/tde-16042012-105910/.
Повний текст джерелаАнотація:
O presente trabalho teve como objetivos verificar os efeitos da radiação gama em grãos de milho contaminados artificialmente com Aspergillus flavus Link produtor de aflatoxinas; demonstrar a aplicação da técnica da Reação em Cadeia da Polimerase (PCR) no diagnóstico de A. flavus, bem como verificar o efeito da radiação no perfil das bandas de DNA. Vinte amostras de grãos de milho com 200 g cada foram irradiadas individualmente com 20 kGy, para eliminar a contaminação microbiana. Em seguida, as amostras foram inoculadas com A. flavus toxigênico (1 x 106 esporos / ml), incubadas por 15 dias a 25 °C em ambiente com umidade relativa ao redor de 97,5% e irradiadas com 0; 2; 5 e 10 kGy. As amostras, 5 para cada dose de irradiação, foram analisadas individualmente quanto ao número de células fúngicas, atividade de água, teste de viabilidade (diacetato de fluoresceína e brometo de etídio), PCR e detecção de aflatoxinas (AFB). Os resultados demonstraram que as doses utilizadas foram efetivas na redução do número de Unidades Formadoras de Colônias (UFC/g), principalmente as doses de 5 e 10 kGy. Em adição, o teste de viabilidade mostrou uma diminuição de células viáveis com o aumento das doses de irradiação. A redução de AFB1 e AFB2 foi mais eficiente com o emprego de 2 kGy, comparativamente à dose de 5 kGy, enquanto a dose de 10 kGy degradou totalmente as aflatoxinas. Além disso, observou-se que AFB2 apresentou-se mais radiosensível. O emprego da técnica de PCR revelou a presença de bandas de DNA em todas as amostras.<br>The aim of this present study was to verify the effects of gamma radiation on the growth of Aspergillus flavus Link aflatoxins producer; to demonstrate the application of Polymerase Chain Reaction (PCR) technique in the diagnostic of A. Flavus, as well to verify the effect of radiation in the profile of DNA bands. Twenty samples of grains maize with 200 g each were individually irradiated with 20 kGy, to eliminate the microbial contamination. In following, the samples were inoculated with an toxigenic A. flavus (1x106 spores/ml), incubated for 15 days at 25 °C with a relative humidity of around 97,5% and irradiated with 0; 2; 5 and 10 kGy. The samples, 5 to each dose of irradiation, were individually analyzed for the number of fungal cells, water activity, viability test (fluorescein diacetate and ethidium bromide), PCR and aflatoxins (AFB) detection. The results showed that the doses used were effectives in reducing the number of Colony Forming Units (CFU/g) mainly the doses of 5 and 10 kGy. In addition, the viability test showed a decrease of viable cells with increase of irradiation doses. The reduction of AFB1 and AFB2, was more efficient with the use of 2 kGy in comparison with the dose of 5 kGy, while the dose of 10 kGy, degraded the aflatoxins. Thereby, it was observed that AFB2 showed to be more radiosensitive. The use of PCR technique showed the presence of DNA bands, in all samples
37
Playle, Laura Charlotte. "Radiation-induced apoptosis and cell cycle checkpoints in human colorectal tumour cell lines." Thesis, University of Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341501.
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38
Milián, Félix Más. "Estudo in vitro dos efeitos radiobiológicos no DNA plasmidial com radiações ionizantes de baixo LET." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/43/43134/tde-04122006-150637/.
Повний текст джерелаАнотація:
O estudo da interação da radiação com moléculas de DNA tem se intensificado nos últimos anos, determinando avanços nas técnicas experimentais e na compreensão teórica desse fenômeno. No entanto, falta ainda um estudo sistemático e com boa precisão da interação de diferentes radiações com o DNA em condições controladas. Neste trabalho desenvolveu-se uma técnica experimental que permite o estudo daquela interação com diferentes radiações, permitindo uma análise quantitativa dos efeitos da radiação sobre o DNA, mais especificamente, da produção de single- e double strand breaks em moléculas de DNA plasmidial irradiados em solução aquosa com diferentes concentrações de scavengers. Para o desenvolvimento desse trabalho, foram realizados diversos testes para encontrar as condições ideais para se reduzir as incertezas na quantificação das diferentes quebras no DNA. Desenvolveu-se também um programa computacional que permite uma análise precisa da imagem da eletroforese, que oferece ferramentas úteis para a análise quantitativa. Com isso, reduziram-se as incertezas e flutuações experimentais, o que permitiu o estudo da interação radiação-DNA em condições de concentrações de scavengers muito baixas. Os resultados são compatíveis com os dados experimentais, nas condições onde estes já existiam, e compatíveis com o esperado teoricamente nas condições onde não existem dados experimentais para a comparação<br>The interaction of radiation with DNA molecules has been intensively studied in the last years, allowing improvements on the experimental techniques and on the theoretical comprehension of the phenomena involved in that interaction under controlled conditions. In this work, a new experimental technique has been developed which enables one to study the radiation-DNA interaction for different radiations and with reduced uncertainties, allowing a quantitative analysis of single- and double-strand breaks on DNA in aqueous solutions with different scavenger concentrations. To this end, many experimental tests were performed in order to find the best experimental condition for reducing the uncertainties. A software was developed for quantitative analysis of the electrophorese image, offering the most important tools for accurate quantification of the DNA products. An important reduction on uncertainties was achieved, allowing the extension of experimental studies to the low scavenger concentration region. The results are in good agreement with experimental data at those conditions where these experiments were already performed, and in agreement with the theoretical model where there are no experimental results to compare with.
39
Gulston, Melanie Katharine. "The effects of the sunscreen chemicals Padimate-O and 2-ethylhexyl-P-methoxycinnamate on DNA." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301520.
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40
Sirzén, Florin. "Molecular aspects of cellular radiosensitivity in small cell lung carcinoma /." Stockholm, 1998. http://diss.kib.ki.se/1998/19981204sirz/.
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41
Saul, Alison Nicole. "Psycho-physiological stress and its effects on ultraviolet light induced inflammation, DNA damage, and skin carcinogenesis." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1172850801.
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Terry, Samantha Y. A. "A role for topoisomerase II alpha in chromosome damage in human cell lines." Thesis, University of St Andrews, 2010. http://hdl.handle.net/10023/873.
Повний текст джерелаАнотація:
Human response to ionising radiation (IR) shows a wide variation. This is most clearly seen in the radiation-response of cells as measured by frequencies of chromosomal aberrations. Different frequencies of IR-induced aberrations can be conveniently observed in phytohaemagglutin-stimulated peripheral blood T-lymphocytes from both normal individuals and sporadic cancer cases, in either metaphase chromosomes or as micronuclei in the following cell cycle. Metaphase cells show frequent chromatid breaks, defined as chromatid discontinuities or terminal deletions, if irradiated in the G 2 -phase of the cell cycle. It has been shown that the frequency of chromatid breaks in cells from approximately 40% of sporadic breast cancer patients, are significantly higher than in groups of normal individuals. This suggests that elevated radiation-induced chromatid break frequency may be linked with susceptibility to breast cancer. It is known that chromatid breaks are initiated by a double strand break (DSB), but it appears that the two are linked only indirectly as repair kinetics for DSBs and chromatid breaks do not match. Therefore, the underlying causes of the wide variation in frequencies of chromatid breaks in irradiated T-lymphocytes from different normal individuals and from sporadic breast cancer cases are still unclear but it is unlikely to be linked directly to DSB rejoining. My research has focused on the mechanism through which chromatid breaks are formed from initial DSBs. The lack of a direct association suggested that a signalling process might be involved, connecting the initial DSB and resulting chromatid break. The signal model, suggested that the initial DSB is located within a chromatin loop that leads to an intra- or interchromatid rearrangement resulting in incomplete mis-joining of chromatin ends during the decatenation of chromatids during G 2 . It was therefore proposed that topoisomerase II alpha (topo IIα) might be involved, mainly because of its ability to incise DNA and its role in sister chromatid decatenation. During my PhD research I have used a strategy of altering topo II activity or expression and studying whether this alters IR-induced chromatid break frequency. The first approach involved cell lines that varied in topo IIα expression. The frequency of IR-induced chromatid breaks was found to correlate positively with topo IIα expression level, as measured in three different cell lines by immunoblotting, i.e. two cell lines with lower topo IIα expression exhibited lower chromatid break frequency. Topo II activity in these three cell lines was also estimated indirectly by the ability of a topo IIα poison to activate the G 2 /M checkpoint, and this related well with topo IIα expression. A second approach involved ‘knocking down’ topo IIα protein expression by silencing RNA (siRNA). Lowered topo IIα expression was confirmed by immunoblotting and polymerase chain reaction. SiRNA-lowered topo IIα expression correlated with a decreased IR-induced chromatid break frequency. In a third series of experiments cells were treated with ICRF-193, a topo IIα catalytic inhibitor. It was shown that inhibition of topo IIα also significantly reduced IR-induced chromatid breaks. I also showed that lowered chromatid break frequency was not due to cells with high chromatid break frequencies being blocked in G 2 as the mitotic index was not altered significantly in cells with lowered topo IIα expression or activity. These experiments show that topo IIα is involved in IR-induced chromatid break formation. The final experiments reported here attempted to show how topo II might be recruited in the process of forming IR-induced chromatid breaks. Hydrogen peroxide was used as a source of reactive oxygen species (reported to poison topo IIα) and it was shown that topo IIα under these conditions is involved in the entanglement of metaphase chromosomes and formation of chromatin ‘dots’ as well as chromatid breaks. Experiments using atomic force microscopy attempted to confirm these dots as excised chromatin loops. The possible role of topo IIα in both radiation- and hydrogen peroxide-induced primary DNA damage was also tested. It was shown that topo IIα does not affect radiation-induced DSBs, even though it does affect chromatid break frequency. Also, topo IIα does not affect hydrogen peroxide-induced DNA damage at low doses. The results support the idea that topo IIα is involved in the conversion of DSBs to chromatid breaks after both irradiation and treatment with hydrogen peroxide at a low concentrations. I have demonstrated that topo IIα is involved in forming IR-induced chromatid breaks, most likely by converting the initial DSBs into chromosomal aberrations as suggested by the signal model.
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Valgôde, Flávia Gomes Silva. "Avaliação do dano radioinduzido, capacidade de reparo e morte cecular em células humanas tumorais (T-47D e MCF-7) e não tumorais (MCF-10) de mama." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/85/85131/tde-16052012-141727/.
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Câncer de mama é considerado uma das malignidades mais comuns que acometem as mulheres, representando cerca de uma em cada três de todas as neoplasias femininas. Aproximadamente, 90% dos casos de câncer de mama são esporádicos, atribuíveis aos eventos somáticos e cerca de 10% estão associados com a história familial e destes somente 4-5% são decorrentes de fatores hereditários. Em clínica, a radiação ionizante é a principal ferramenta utilizada no controle do crescimento tumoral, além da intervenção cirúrgica e quimioterapia. Há, no entanto, poucas infomnações no que diz respeito a resposta celular frente à ação da radiação ionizante em células-alvo, isto é, em linhagens celulares originárias de câncer de mama. O presente estudo foi proposto para analisar a radiossensibilidade de células humanas tumorals (T-47D e MCF-7) e não tumorals (MCF-10), originárias de mama, submetidas a várias doses (0,5 a 30 Gy) de radiação y de 60Co (0,72 - 1,50 Gy/min). Para tanto, foram utilizados como parâmetros de radiossensibilidade, dano radioinduzido ao DNA, capacidade de reparo e morte celular, por meio das técnicas do micronúcleo, eletroforese de microgel (teste do cometa) e viabilidade celular. Os dados obtidos mostraram que as linhagens tumorais (T-47D e MCF-7) foram mais radiossensíveis que a linhagem não tumoral (MCF-10) para todos os testes utilizados. A linhagem T-47D foi a que apresentou uma maior quantidade de dano radioinduzido, um ciclo celular mais acelerado e uma maior taxa de morte celular. As três linhagens celulares apresentaram uma capacidade de reparo relativamente eficiente, tendo em vista que uma hora após a irradiação, todas elas exibiram uma redução considerável de dano radioinduzido quando comparadas logo após as exposições. Os testes empregados mostraram ser seguros, sensíveis e reprodutíveis e permitiram quantificar e avaliar danos induzidos ao DNA, capacidade de reparo e morte celular, nas três linhagens originárias de mama humana.<br>Breast cancer is one of the most common malignancies that account women, representing about one in three of all female neoplasm. Approximately, 90% of cases are considered sporadic, attributed to somatic events and about 10% have a family history and this only 4 - 5 % is decurrent of hereditary factors. In the clinic, ionizing radiation is a major tool utilized in the control of tumour growth, besides surgery and chemotherapy. There is, however, little information concerning cellular response to the action of ionizing radiation in the target cells, i.e., cell lines originating from breast cancer. The present study proposed to analyze the radiosensitivity of the human tumorigenic (T-47D and MCF-7) and nontumorigenic (MCF-10) cell lines, originating from breast and submitted to various doses (0.5 to 30 Gy) of 60Co rays (0.72 - 1.50 Gy/min). For this purpose, DNA radioinduced damage, repair capacity and cell death were utilized as parameters of radiosensitivity by micronucleus, single cell gel electrophoresis (Comet assay) and cell viability techniques. The data obtained showed that tumorigenic cell lines were more radiosensitive than nontumorigenic breast cells in all assays here utilized. The T-47D cell line was presenting the highest amount of radioinduced damage, a more accelerated proliferation rate and a higher rate of cell death. The three cell lines presented a relatively efficient repair capacity, since one hour after the irradiation all of them showed a considerable reduction of radioinduced damage. The techniques employed showed to be secure, sensitive and reproducible, allowing to quantify and evaluate DNA damage, repair capacity and cell death in the three human breast cell lines.
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Mahee, Durude. "Numerical Simulation and Graphical Illustration of Ionization by Charged Particles as a Tool toward Understanding Biological Effects of Ionizing Radiation." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535381068931831.
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MELO, ANA M. M. de A. "Estudos dos efeitos da radiacao gama de sup60Co sobre larvas de Biomphalaria glabrata (Say,1818)." reponame:Repositório Institucional do IPEN, 1998. http://repositorio.ipen.br:8080/xmlui/handle/123456789/9270.
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Connelly, Sandra J. "Effects of Ultraviolet Radiation (UVR) Induced DNA Damage and Other Ecological Determinants on cryptosporidium Parvum, Giardia Lamblia, and Daphnia spp. in Freshwater Ecosystems." Oxford, Ohio : Miami University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=miami1196353326.
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Fourie, Hein. "Microdosimetric studies of Auger electrons from DNA-incorporated 123-I using the micronucleus assay and the Geant4 Monte Carlo simulation tookit." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/95801.
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Thesis (MSc)--Stellenbosch University, 2014.<br>ENGLISH ABSTRACT: This study’s focus is on the determination and quantization of radiation damage on a cellular level due to the decay of the Auger electron-emitting 123I and the replication of this energy deposition using Geant4 Monte Carlo simulations. The relatively short half-life of 123I (13.2 hours) makes it ideal for studies of Auger electrons which induce biological damage similar to that of high linear energy transfer radiations, when permitted to deposit their energy in close proximity to DNA. Due to small cellular dimensions, direct dose measurements are impossible but estimates may be made from Monte Carlo simulations. In this investigation the thymidine analogue 5-[123I]-iodo-2-deoxyuridine (123IUdR) was used to incorporate the 123I into the cellular DNA of T-lymphocytes from two human donors. Radiation induced micronuclei were numerated in binucleated cells using fluorescence microscopy. The energy deposition per decay of 123I was calculated within a spherical geometry, having the same size and density as a human lymphocyte, using the open source Geant4 toolkit. The absorbed energy per disintegration was used to convert the incorporated 123I activity (Bq) into absorbed dose (Gy) values, in order to compare the biological damage caused by the radioactive iodine to 60Co γ-radiation. A linear relationship between micronuclei frequency and 123I activity could be established. The linear dose-response noted for Auger electrons in the study is indicative of the high-LET nature of these particles. Using the linear-quadratic dose-response curve for micronuclei frequencies following exposure to graded doses of 60Co γ-rays, the relative biological effectiveness (RBE) of the DNA incorporated 123I estimated in this work was found to range from 19 ± 10 to 32 ± 7 for lymphocyte donor 1 and 15 ± 6 to 42 ± 11 for donor 2. The dose limiting RBE (RBEM) for lymphocyte donor 1 and 2 are respectively 34 ± 8 and 50 ± 15 and follows the expected shift in terms of the inherent radiosensitivity of the donors. We also considered the inclusion of the S-phase fraction of the lymphocytes in the dosimetry calculations. The resultant RBEs of the dose points of lymphocyte donor 1 ranges from 4 ± 2 to 7 ± 2, and those of donor 2 ranges from 3 ± 1 to 9 ± 2. The RBEM for lymphocyte donor 1 and 2 are respectively 7 ± 2 and 11 ± 3. The inclusion of the S-phase fraction reduces the calculated RBEs significantly and these observed RBE values relate well to those obtained in studies with fibroblasts and 125IUdR.<br>AFRIKAANSE OPSOMMING: Hierdie studie fokus op die bepaling en kwantisering van stralingskade op 'n sellulêre vlak as gevolg van die verval van 123I wat Auger elektrone afgee, asook die simulering van hierdie energie afsetting met behulp van die Geant4 Monte Carlo program. Die relatiewe kort half-leeftyd van 123I (13.2 uur) maak dit ideaal vir studies van Auger elektrone wat biologiese skade soortgelyk aan dié van 'n hoë lineêre-energie-oordrag uitstraling veroorsaak, indien die energie van die elektrone naby sellulêre DNA geabsorbeer word. As gevolg van die klein sellulêre dimensies is direkte dosis metings egter onmoontlik, maar skattings kan gemaak word met behulp van Monte Carlo simulasies. Die timidien analoog 5-[123I]-jodo-2-deoxyuridien (123IUdR) was in hierdie ondersoek gebruik om die 123I in die DNA van menslike T-limfosiete in te bou. Mikrokerne in dubbel-kernige selle wat vorm as gevolg van die Auger elektrone was getel met behulp van fluoressensie mikroskopie. Die energie afsetting per 123I verval was bereken binne ‘n sferiese geometrie, met dieselfde grootte en digtheid as 'n menslike limfosiet, met behulp van die Geant4 sagteware. Die geabsorbeerde energie per verval was gebruik om die geïnkorporeerde 123I aktiwiteit (Bq) om te skakel na ‘n waarde van geabsorbeerde dosis (Gy), ten einde die biologiese skade wat veroorsaak word deur die radioaktiewe jodium-123 met kobalt-60 gamma straling te vergelyk. ‘n Lineêre verwantskap tussen die mikrokerne frekwensies en die 123I aktiwiteit is vasgestel. Hierdie verwantskap vir Auger elektrone is 'n aanduiding van die hoë lineêre-energie-oordrag van hierdie deeltjies. Die lineêr-kwadratiese dosis-effek krommes vir mikrokerne frekwensies na blootstelling aan 60Co γ-strale was gebruik om die relatiewe biologiese doeltreffendheid (RBE) van die DNA geïnkorporeerde 123I te beraam. RBE waardes wissel van 19 ± 10 tot 32 ± 7 vir limfosiete van skenker 1 en 15 ± 6 tot 42 ± 11 vir skenker 2. Die dosis beperkte RBE (RBEM) vir limfosiet skenker 1 en 2 is onderskeidelik 34 ± 8 en 50 ± 15 en volg die verwagte skuif in terme van die inherente radiogevoeligheid van die skenkers. Die fraksie van limfosiete wat in S-fase was tydens die blootstelling aan 125IUdR was ingesluit in verdere dosimetrie berekeninge. Die gevolglike RBEs van die dosispunte van limfosiete van skenker 1 wissel van 4 ± 2 tot 7 ± 2 en dié van skenker 2 wissel van 3 ± 1 tot 9 ± 2. Die RBEM vir limfosiet skenker 1 en 2 is onderskeidelik 7 ± 2 en 11 ± 3. Die insluiting van die S-fase fraksie verminder die berekende RBEs aansienlik en die RBE waardes waargeneem hou goed verband met die wat in studies met fibroblaste en 125IUdR verkry is.
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von, Koschembahr Anne M. "Endothelin-1 Protects Human Melanocytes from the Photodamaging Effects of Ultraviolet Radiation by Activating the MAP Kinases JNK and p38." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1418909421.
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Gould, Richard. "An investigation of scatter removal techniques in paediatric cardiac catheterisation imaging: effects upon radiation dose, image quality DNA integrity and cancer risk." Thesis, Ulster University, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680142.
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TALLARICO, LENITA de F. "Avaliacao dos efeitos toxicos e mutagenicos de amostras ambientais do Rio Tiete na regiao de Suzano em Biomphalaria glabrata (SAY, 1818)." reponame:Repositório Institucional do IPEN, 2009. http://repositorio.ipen.br:8080/xmlui/handle/123456789/9382.
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Made available in DSpace on 2014-10-09T12:26:23Z (GMT). No. of bitstreams: 0<br>Made available in DSpace on 2014-10-09T14:04:24Z (GMT). No. of bitstreams: 0<br>Tese (Doutoramento)<br>IPEN/T<br>Instituto de Pesquisas Energeticas e Nucleares - IPEN-CNEN/SP