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At least 199 records · Page 11Linked to original sources
PubMed2002

Do low dose-rate bystander effects influence domestic radon risks?

PURPOSE: Radon risks derive from exposure of bronchio-epithelial cells to high-linear energy transfer (LET) alpha-particles. alpha-particle exposure can result in bystander effects, where irradiated cells emit signals resulting in damage to nearby unirradiated bystander cells. This can result in non-linear dose-response relations, and inverse dose-rate effects. Domestic radon risk estimates are currently extrapolated from miner data, which are at both higher doses and higher dose-rates, so bystander effects on unhit cells could play a large role in the extrapolation of risks from mines to homes. Therefore, we extend an earlier quantitative mechanistic model of bystander effects to include protracted exposure, with the aim of quantifying the significance of the bystander effect for very prolonged exposures. MATERIALS AND METHODS: A model of high-LET bystander effects, originally developed to analyse oncogenic transformation in vitro, is extended to low dose-rates. The model considers radiation response as a superposition of bystander and linear direct e It attributes bystander effects to a small subpopulation of hypersensitive cells, with the bystander contribution dominating the direct contribution at very low acute doses but saturating as the dose increases. Inverse dose-rate effects are attributed to the replenishment of the hypersensitive subpopulation during prolonged irradiation. RESULTS: The model was fitted to dose- and dose-rate-dependent radon-exposed miner data, suggesting that one directly hit target bronchio-epithelial cell can send bystander signals to about 50 neighbouring target cells. The model suggests that a naïve linear extrapolation of radon miner data to low doses, without accounting for dose-rate, would result in an underestimation of domestic radon risks by about a factor of 4, a value comparable with the empirical estimate applied in the recent BEIR-VI report on radon risk estimation. CONCLUSIONS: Bystander effects represent a plausible quantitative and mechanistic explanation of inverse dose-rate effects by high-LET radiation, resulting in non-linear dose-response relations and a complex interplay between the effects of dose and exposure time. The model presented provides a potential mechanistic underpinning for the empirical exposure-time correction factors applied in the recent BEIR-VI for domestic radon risk estimation.

Air Pollution, Indoor↗
PubMed1997

Mutation frequency of Dictyostelium discoideum spores exposed to the space environment.

Two strains of cellular slime mold Dictyostelium discoideum, a radiosensitive mutant and the parental wild-type strain, were used to investigate the effects of cosmic radiation on viability and mutation frequency at the spore stage for about 9 days in Space Shuttle of NASA. We measured little effect of space environment on viability and cell growth in the both strains as compared to ground controls. The mutation frequency of the flown spores were similar to that of ground control. These results suggest that there could be no effect of cosmic radiation, containing high linear energy transfer radiation at about 0.9 mSv/day as detected by real-time radiation monitoring device on the induction of mutation at the spore stage.

Animals↗
PubMed2005

Fragmentation of 1 GeV/nucleon iron ions in thick targets relevant for space exploration.

We have measured charged nuclear fragments produced by 1 GeV/nucleon 56Fe ions interacting with aluminium, polyethylene and lead. These materials are relevant for assessment of radiation risk for manned space flight. The data will be presented in a form suitable for comparison with models of nuclear fragmentation and transport, including linear energy transfer (LET) spectrum, fluence for iron and fragments, event-tack- and event-dose-averaged LET, total dose and iron contribution to dose.

Aluminum↗
PubMed2002

Enhancement of X-ray-induced breaks in DNA bound to molecules containing platinum: a possible application to hadrontherapy.

Complexes made of DNA and chloroterpyridine platinum (PtTC) bound to plasmid DNA were placed in aqueous solution and irradiated with monochromatic X rays tuned to the resonant photoabsorption energy of the L(III) shell of the platinum atom. The number of single- and double-strand breaks (SSBs and DSBs) induced by irradiation on a supercoiled DNA plasmid was measured by the production of the circular-nicked and linear forms. To distinguish the contribution of the direct effects of ionization from the indirect effects due to a free radical attack, experiments were also performed in the presence of a hydroxyl free radical scavenger, dimethyl sulfoxide (DMSO). An enhancement of the number of SSBs and DSBs was observed when the plasmids contained the platinum intercalating molecules. A quantitative analysis was made to evaluate the respective contributions of the direct effects (Auger effect) and the indirect effects (free radical attack) to the number of DNA strand breaks. Even when off-resonant X rays were used, the strand break efficiency remained higher than expected based upon the absorption cross section, suggesting that the platinum bound to DNA might be increasing the yield of strand breaks. A mechanism is suggested that involves photoelectrons generated from the ionization of water which efficiently ionize platinum atoms. If this mechanism is correct, then heavy atoms, with a large cross section for ionization by electrons that are bound to the DNA, should behave as a radiosensitizer. This observation may provide insight into understanding the effects of new radiotherapy protocols, related chemotherapeutic agents such as cisplatin, and conventional radiotherapy for the treatment of tumors. A possible way to deliver the dose selectively in a well-defined volume, which uses the properties of the linear energy transfer of atomic ions interacting with matter, is suggested.

Chromosome Breakage↗
PubMed1995

DNA damage produced by exposure of supercoiled plasmid DNA to high- and low-LET ionizing radiation: effects of hydroxyl radical quenchers.

Production of DNA damage by exposure to ionizing radiation was measured in two in vitro systems. A supercoiled plasmid of 7.3 kbp was isolated and exposed in an aqueous environment to 60Co gamma rays and JANUS 0.85 MeV fission-spectrum neutrons. Dose responses for the production of single-strand breaks (ssbs) and double-strand breaks (dsbs) were computed from the conversion of the supercoil to its relaxed and linear forms. The relative effectiveness (neutrons:gamma-rays) for destruction of genetic transforming activity of M13 viral DNA was 0.23, close to that for ssb production, in contrast with the situation for biological effects such as lethality, mutagenesis and cellular transformation measured in mammalian cells, where RBEs are > 1. The role of hydroxyl (OH) radicals in DNA damage induction by neutrons was investigated by exposure of plasmid in the presence of known quenchers of this species. Of four quenchers tested, all were able to reduce the yields of both ssbs and dsbs. These findings are consistent with a model for ssb and dsb induction by high linear energy transfer radiation that involves OH radical medication.

Acetates↗
PubMed1998

Detection of codon 12 point mutations of the K-ras gene from mouse lung adenocarcinoma by 'enriched' PCR.

PURPOSE: Recent studies have shown that chemical carcinogens induce a high frequency of point mutations in the K-ras oncogene from mouse lung tumours at codons 12, 13 and 61. These experiments were performed to identify K-ras mutations in tissues from control and radiation-exposed mice. MATERIALS AND METHODS: By modifying the technique of the 'enriched' polymerase chain reaction (PCR), it was possible to detect point mutations at codon 12 of the K-ras oncogene from 25-year-old paraffin-embedded normal lungs and lung adenocarcinomas from mice exposed to radiation. Together, a total of 120 lung tissues were screened for point mutations at codon 12 of the K-ras oncogene in this study. RESULTS: A significant increase in K-ras codon 12 point mutations was observed in the normal lungs from mice exposed to 24 once-weekly neutron irradiations (100%), compared with normal lungs from mice with sham-irradiation (50%) (p<0.05). Lung adenocarcinomas from mice receiving 24 once-weekly neutron irradiations also had a significantly higher frequency of K-ras codon 12 point mutations (100%) than the lung adenocarcinomas of mice receiving 24 or 60 once-weekly gamma-ray irradiations (50%), but the higher frequency was not significantly different from that in spontaneous lung adenocarcinomas from mice (75%; p > 0.05). The validity of the technique was confirmed by sequencing two of the mutants. In doing so, a K-ras 13(Asp) point mutation was observed. CONCLUSIONS: The data suggest that high-linear energy transfer (LET) neutron radiation was more effective than low-LET gamma-rays in inducing K-ras point mutations at codon 12 in the lungs of B6CF1 mice.

Animals↗
PubMed1995

Heavy ion-induced DNA double-strand breaks with yeast as a model system.

Cells of diploid yeast, Saccharomyces cerevisiae, were exposed to a variety of energetic heavy ions (provided by the UNILAC facility at the Gesellschaft für Schwerionenforschung, GSI), 241Am alpha-particles and 80-keV x-rays after which they were assessed for DNA double-strand breaks (DSB) using either the neutral sedimentation or the pulsed-field gel electrophoresis (PFGE) technique. Both yielded comparable results. The DSB production cross-sections are compared with inactivation studies performed for the same cells under identical conditions. The measurements show that with lighter ions DSB induction cross-sections increase with linear energy transfer (LET), but the situation is less clear with the heavier ions. A close parallelism was found between DSB induction and cell inactivation in these yeast cells.

Alpha Particles↗
PubMed2004

Changes in G1-phase populations in human glioblastoma and neuroblastoma cell lines influence p66/Be neutron-induced micronucleus yield.

Some photon resistant tumours are sensitive to neutrons but no predictive methods exist which could identify such tumours. In a recent study addressing this clinically important issue, we demonstrated that relative biologic effectiveness (RBE) values for p(66)/Be neutrons estimated from micronucleus (MN) data correlate positively with RBE values obtained from conventional clonogenic survival data. However, not all photon-resistant cell lines showed high RBE values when the MN endpoint was used. Now, we examine how the functional status of the p53 tumour suppressor gene and radiation-induced changes in cell cycle phase populations may contribute to this discrepancy. No significant association was established between p53 status and MN yield for both photon and neutron irradiation. The data demonstrated that neutron-, but not photon-, induced MN yield is dependent on the intrinsic ability of cells to activate a G1-phase arrest. In cell lines of comparable photon sensitivity, those showing more extensive depletion of the G1 population express significantly more micronuclei per unit dose of neutrons. These results suggest that differences in cell cycle kinetics, and not the p53 status, may constitute an important factor in damage induction by high linear energy transfer (LET) irradiation and need to be considered when radiation toxicity in clinical radiobiology or radiation protection is assessed using damage endpoints.

Beryllium↗
PubMed1998

RBE for the induction of apoptosis in human peripheral lymphocytes exposed in vitro to high-LET radiation generated by accelerated nitrogen ions.

PURPOSE: To investigate the relative biological effectiveness (RBE) of accelerated nitrogen ions (32-45 MeV/u) compared with 137Cs gamma-rays for the induction of apoptosis in G0 lymphocytes. MATERIALS AND METHODS: Human peripheral G0 lymphocytes were exposed in vitro to doses up to 3 Gy. RBE for the induction of apoptosis was studied at different times after irradiation (0, 24, 48 and 72 h) with the use of three different methods: (1) morphological characterization of apoptotic cells after fluorescence staining; (2) cell size distribution analysis of the cell population to detect apoptotic bodies; and (3) electrophoretic analysis of DNA to detect 'DNA-ladders'. RESULTS: RBE values in the range of 1.3-3.0 were obtained from the linear components of the dose response curves. The variation in RBE was primarily dependent on post-irradiation time, where the highest RBE values were obtained after 48 h. The three different techniques used for analysis of apoptosis gave similar results. The significantly increased RBE was also seen as an earlier appearance of DNA-ladders, as well as a more rapid disappearance of the total number of viable cells. CONCLUSIONS: These results show that nitrogen ions of high linear energy transfer (LET) produce RBE > 1.0 and induce a faster apoptotic response as compared with gamma-photons of low-LET radiation.

Apoptosis↗
PubMed1995

Quantities and units in radiation protection.

In its Publication No. 60, the International Commission on Radiological Protection (ICRP) introduced a new quantity, the equivalent dose in tissue, HT = sigma R WR DT.R where DT.R is the absorbed dose averaged over the tissue or organ, T, and WR is the radiation weighting factor. The latter depends on the incident radiation, i.e., the type and energy, but is independent of the tissue. On the other hand, a customarily defined quantity, the 'dose equivalent' is maintained (in particular the operational dose-equivalent quantities introduced in ICRU Report 39), but the relationship between the quality factor Q(L) and the linear energy transfer, L, has been redefined. In the case of neutrons, this procedure gives rise to an increase of the corresponding fluence to dose-equivalent conversion factors. The reasons for introducing these and the new tissue-weighting factor changes are discussed.

Animals↗
PubMed2002

Modelling the effect of incorporated halogenated pyrimidine on radiation-induced DNA strand breaks.

PURPOSE: To estimate the enhancement of DNA strand breaks induced by low linear energy transfer (LET) radiation in the presence of halogenated pyrimidines and to examine complexity and clustering properties of damage that could provide a correlation between DNA damage and lethality. MATERIALS AND METHODS: Monte Carlo track structure methods were used to model and estimate the induction of strand breakage by X-ray photons with and without the incorporated Br/I deoxyuridine in cell-mimetic conditions. The increase of DNA strand break induction was modelled by taking into account the direct energy deposition and the reactions of radicals. The yield and spectrum of strand breaks were calculated at various degrees of Br/IdU incorporation. The excess strand breaks due to Br/IdU incorporation was assumed to be induced by highly reactive uracilyl radicals. Four mechanisms were considered for the production of uracilyl radicals classified into three groups, by hydrated electrons, by direct energy deposition, and by both hydrated electrons and direct energy depositions. In total, nine different models were considered to test the excess strand breaks by incorporated Br/IdU assuming different pathways. RESULTS: Model calculations show the following: the yield of strand breaks is enhanced by both the e(aq)(-) reaction and the direct energy deposition on base moiety; there is a significant contribution to the enhancement of yield of strand breaks due to energy transfer about four bases along the DNA to Br/IdU and DNA strand break complexity increases with degree of Br/IdU incorporation. Enhancement ratios of 1.8 and 2.5 for 40% Br/IdU substitution were obtained for single- and double-strand breaks, respectively. CONCLUSIONS: The increase in the yield of strand breaks due to Br/IdU incorporation could be explained by the mechanism of uracilyl radical production by e(aq)(-) and direct energy deposition. The importance of energy transfer along the DNA is demonstrated. It is shown that the incorporation of Br/IdU causes a spectral shift towards a greater complexity of clustered DNA damage.

Base Sequence↗
PubMed2002

Response of a tissue equivalent proportional counter to neutrons.

The absorbed dose as a function of lineal energy was measured at the CERN-EC Reference-field Facility (CERF) using a 512-channel tissue equivalent proportional counter (TEPC), and neutron dose equivalent response evaluated. Although there are some differences, the measured dose equivalent is in agreement with that measured by the 16-channel HANDI tissue equivalent counter. Comparison of TEPC measurements with those made by a silicon solid-state detector for low linear energy transfer particles produced by the same beam, is presented. The measurements show that about 4% of dose equivalent is delivered by particles heavier than protons generated in the conducting tissue equivalent plastic.

Dose-Response Relationship, Radiation↗
PubMed1997

Risk assessment for heavy ions of parts tested with protons.

An internuclear cascade-evaporation code is used to model energy deposition in thin slabs of silicon. This model shows that protons produce a significant number of events with effective Linear Energy Transfer (LET) greater than 8 MeV cm2/mg and demonstrates that proton testing of microelectronic components can be an effective way to screen devices for low earth orbit susceptibility to heavy ions.

Computer Simulation↗
PubMed2002

Clustered DNA damages induced in human hematopoietic cells by low doses of ionizing radiation.

Ionizing radiation induces clusters of DNA damages--oxidized bases, abasic sites and strand breaks--on opposing strands within a few helical turns. Such damages have been postulated to be difficult to repair, as are double strand breaks (one type of cluster). We have shown that low doses of low and high linear energy transfer (LET) radiation induce such damage clusters in human cells. In human cells, DSB are about 30% of the total of complex damages, and the levels of DSBs and oxidized pyrimidine clusters are similar. The dose responses for cluster induction in cells can be described by a linear relationship, implying that even low doses of ionizing radiation can produce clustered damages. Studies are in progress to determine whether clusters can be produced by mechanisms other than ionizing radiation, as well as the levels of various cluster types formed by low and high LET radiation.

Cell Line↗
PubMed2004

Induction of reproductive cell death and chromosome aberrations in radioresistant tumour cells by carbon ions.

PURPOSE: To study the induction of reproductive cell death and chromosome aberrations in radioresistant tumour cells exposed to carbon ions in vitro. MATERIALS AND METHODS: X-ray-resistant colon carcinoma cells (WiDr) were used. Confluent G0/G1 cells were irradiated in vitro with graded doses of 100/200/400 MeV u(-1) carbon ions and carbon ions from the middle of a 1 cm extended Bragg peak, and 200 kV X-rays for comparison. Cells were harvested in their first post-irradiation division and aberrations were analysed either by the Giemsa/Hoechst 33258-staining technique or by the fluorescent in-situ hybridization technique involving whole chromosome hybridization and 4',6-diaminido-2-phenylidole (DAPI)-staining. Whole chromosome probes were used for chromosomes 2, 4 and 5, and the chromosome painting patterns were classified according published protocols. Reproductive cell survival was determined by a standard clonogenic assay. RESULTS: With respect to the induction of reproductive cell death and chromosome aberrations, carbon ions of different energies were more effective than 200 kV X-rays. As expected, irradiation in the extended Bragg peak was the most efficient mode. For cell killing, relative biological effectiveness increased with linear energy transfer up to 2.9. The frequencies of total dicentrics and excess acentric fragments as determined in Giemsa-stained cells were higher in cells irradiated with carbon ions than in cells with X-rays. For 100 MeV u(-1) ions, the dose dependence of apparently simple dicentrics as determined for chromosomes 2, 4 and 5 by single-colour fluorescent in-situ hybridization was linear up to 4 Gy, and linear-quadratic for excess acentric fragments and apparently simple translocations. After irradiation with D=4 Gy carbon ions with energy of 100 MeV u(-1) and from the extended Bragg peak, 12 and 54% of cells displayed complex exchanges, respectively. In contrast, after irradiation with D=4 Gy X-rays, only 1% of cells displayed complex aberrations. Hence, the number of cells with complex exchange aberrations increased strongly after irradiation with carbon ions. CONCLUSION: An increased biological efficiency of carbon ions could be confirmed in radioresistant tumour cells with respect to the induction of reproductive cell death and of unstable as well as stable chromosome aberrations. Relative biological effectiveness reached 2.9 for cell killing by carbon ions from the extended Bragg peak. The yields of apparently simple dicentrics as well as of total dicentrics, i.e. simple dicentrics plus dicentrics belonging to complex exchanges, evaluated in Giemsa-stained metaphases as observed in first post-irradiation mitoses were rather low. In contrast, apparently simple translocations displayed yields systematically higher than simple dicentrics in WiDr cells irradiated with either X-rays or 100 MeV u(-1) or Bragg peak carbon ions. Frequencies o f cells containing complex aberrations increased dramatically after carbon ion irradiation, reaching a maximum for ions from the extended Bragg peak.

Carbon↗
PubMed1995

Induction of micronuclei in plant cells after exposure to accelerated ion irradiation.

The root apex cells of Pisum sativum were irradiated in an U-240 isochronous cyclotron at the Institute for Nuclear Research of the Ukrainian National Academy of Sciences, Kyiv. Several types of micronuclei, differing in structural peculiarities, were observed in the 84 h following exposure to beams of accelerated 1H, 4He, and 14N ions with linear energy transfer (LET) of 0.95, 9.34, and 221 keV/microns, respectively. The maximum micronucleus induction was observed after irradiation with helium ions. Results obtained show that the micronucleus assay is a responsive test for investigations of cytogenetic damage produced by high LET beams in dividing cell systems in vivo.

Linear Energy Transfer↗
PubMed1995

Dosimetric results on EURECA.

Detector packages were exposed on the European Retrievable Carrier (EURECA) as part of the Biostack experiment inside the Exobiology and Radiation Assembly (ERA) and at several locations around EURECA. The packages consist of different plastic nuclear track detectors, nuclear emulsions and thermoluminescence dosimeters (TLDs). Evaluation of these detectors yields data on absorbed dose and particle and linear energy transfer (LET) spectra. Behind a shielding thickness in front of the detectors of 0.09g cm-2 the doses range between 21.26 Gy and 0.87 Gy depending on the location of the dosimeter. Not all measurement can be explained by calculations.

Cosmic Radiation↗
PubMed2003

Relative implications of protective responses versus damage induction at low dose and low-dose-rate exposures, using the microdose approach.

In reviewing the tissue effects of low-dose radiation (1) absorbed dose to tissue is replaced by the sum of energy deposited with track events in cell-equivalent tissue micromasses, i.e. with microdose hits, in the number of exposed micromasses and (2) induced cell damage and adaptive protection are related to microdose hits in exposed micromasses for a given radiation quality. DNA damage increases with the number of microdose hits. They also can induce adaptive protection, mainly against endogenous DNA damage. This protection involves cellular defences, DNA repair and damage removal. With increasing numbers of low linear energy transfer (LET) microdose hits in exposed micromasses, adaptive protection first tends to outweigh damage and then (above 200 mGy) fails and largely disappears. These experimental data predict that cancer risk coefficients derived by epidemiology at high-dose irradiation decline at low doses and dose rates when adaptive protection outdoes DNA damage. The dose-risk function should include both linear and non-linear terms at low doses.

Adaptation, Physiological↗