Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “IONIZATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,063 records · Page 59Linked to original sources
PubMed2006

Photoelectron imaging of propanal by resonant multiphoton ionization via the 3s Rydberg state.

We report the conformationally- and vibrationally-selected photoelectron spectroscopy of propanal obtained by resonance-enhanced multiphoton ionization (REMPI) using photoelectron imaging. These photoelectron spectra, employing (2 + 1) ionization via the (n, 3s) Rydberg transitions in the range from 365 to 371 nm, confirm that there are two stable conformer origins in the lowest ionic state, the cis conformer with a co-planar CCCO geometry and a gauche conformer with a approximately 119 degrees CCCO dihedral angle. From ab initio calculations at the B3LYP/6-311++G** level, we find the gauche conformer is slightly more stable, with the energy difference between two conformers determined to be only 65 cm(-1). In our photoelectron spectra, the vertical ionization potential (IP) for the cis conformer of propanal was then determined to be 9.999 (+/-0.003) eV, while that of the gauche conformer of propanal was estimated to be 9.944 eV. A long vibrational progression in the in-plane CCCO deformation vibrational mode, v, for the cis conformer is systematically observed in all photoelectron spectra in which this mode is excited, suggesting that the geometry of the ground ionic state is significantly different from that of the 3s Rydberg state, particularly along the v(15) coordinates.

Aldehydes↗
PubMed1995

Effect of ionizing radiation on AP-1 binding activity and basic fibroblast growth factor gene expression in drug-sensitive human breast carcinoma MCF-7 and multidrug-resistant MCF-7/ADR cells.

We studied the effect of ionizing radiation on the activation of the AP-1 transcription factors and the regulation of basic fibroblast growth factor (bFGF) gene expression in drug-sensitive human breast carcinoma (MCF-7) cells and its drug-resistant variant (MCF-7/ADR) cells. Northern blot and gel mobility shift assays showed that 135 cGy of ionizing radiation induced c-jun and c-fos gene expression, AP-1 binding activity, as well as bFGF gene expression in MCF-7/ADR cells. In MCF-7 cells, however, we observed little/no induction of bFGF gene expression and AP-1 binding activity after the stress. Nevertheless, MCF-7 cells transfected with plasmids containing c-jun gene contain high levels of bFGF protein. H-7 (60 micrograms/ml), a potent protein kinase C (PKC) inhibitor, inhibited the stress-induced AP-1 binding activity and bFGF gene expression in MCF-7/ADR cells. Corroborating this observation, overexpression of PKC alpha induced bFGF gene expression in MCF-7 cells. Taken together, these results suggest that stress-induced bFGF gene expression is mediated through the activation of PKC and AP-1 transcription factors. Differences in the levels of PKC activity and AP-1 binding factors may be responsible for differential expression of bFGF among breast cancer cell lines. Although there are large differences in response to ionizing radiation between MCF-7 and MCF-7/ADR cell lines, we observed no significant differences in radiocytotoxicity between them.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2001

Role of ATM in oxidative stress-mediated c-Jun phosphorylation in response to ionizing radiation and CdCl2.

Ionizing radiation-induced phosphorylation of the transcription factor c-Jun is impaired in cells derived from individuals with ataxia telangiectasia (AT), in which the ATM gene is mutated. We demonstrate here that ATM modulates c-Jun phosphorylation following exposure to ionizing radiation as well as treatment with CdCl(2), a potent pro-oxidant. Exposure of AT and control fibroblasts to CdCl(2) induced a biphasic increase in c-Jun phosphorylation on serine residues 63 and 73, with the extent of the second phase being markedly greater in AT cells than in control cells. Heme oxygenase-1, a marker of oxidative stress, was also significantly induced in AT fibroblasts. Expression of recombinant ATM in AT fibroblasts, however, reduced the extent of the effects of CdCl(2) on both c-Jun phosphorylation and heme oxygenase-1 induction. Our data suggest that ATM contributes to oxidative stress-mediated signaling that leads to c-Jun phosphorylation by acting as a sensor of ionizing radiation-induced oxidative stress and by modulating intracellular redox homeostasis.

Ataxia Telangiectasia Mutated Proteins↗
PubMed2001

Reaction of guanyl radicals in plasmid DNA with biological reductants: chemical repair of DNA damage produced by the direct effect of ionizing radiation.

PURPOSE: It has been previously argued that the use of the one-electron oxidants (SCN)2(*-) and Br2(*-) with plasmid DNA leads to the formation of DNA guanyl radicals. These guanyl radical species are intermediates in the DNA damage produced by processes such as photo-ionization and ionizing irradiation. The present paper evaluates the use of thallium(II) ions (Tl(II)OH(+)) as the one-electron oxidant, and also determines rate constants for the reduction (repair) of guanyl radicals in plasmid DNA by a variety of reducing agents including the biologically important compounds ascorbate and glutathione. MATERIALS AND METHODS: Aqueous solutions of plasmid DNA containing 10(-3) mol dm(-3) thiocyanate or thallous ions and a reducing agent (azide, nitrite, ferrocyanide, hexachloroiridate(III), iodide, ascorbate, glutathione, glutathione disulphide, methionine, tyrosine, 5-hydroxyindole-3-acetic acid, 10(-7)-10(-4) mol dm(-3)) were irradiated with 137Cs gamma-rays (662 keV). After irradiation, the plasmid was incubated with the E. coli base excision repair endonuclease formamidopyrimidine-DNA N-glycosylase (FPG). Strand break yields after incubation were quantified by means of agarose gel electrophoresis. RESULTS: High yields of FPG-sensitive sites produced by the oxidants (SCN)2(*-) and Tl(II)OH(+) were strongly attenuated by the presence of the reducing agents. CONCLUSIONS: From the results, it is possible to arrive at estimates of the rate constants for the reduction of the DNA guanyl radical by the reducing agents. Values lie in the range 10(4)-10(7) dm(3) mol(-1) s(-1). Using the values for ascorbate and glutathione, it is possible to estimate an upper limit on the order of milliseconds for the lifetime of DNA guanyl radicals under cellular conditions. The implication is that there may well be a significant chemical repair of DNA base damage by the direct effect of ionizing radiation.

DNA↗
PubMed2004

Chromosome aberrations and cell inactivation induced in mammalian cells by ultrasoft X-rays: correlation with the core ionizations in DNA.

PURPOSE: To study the frequency of chromosome aberrations induced by soft X-rays. To see if the core ionization of DNA atoms is involved in this end-point as much as it appears to be in cell killing. MATERIALS AND METHODS: V79 hamster cells were irradiated by synchrotron radiation photons iso-attenuated in the cell (250, 350, 810eV). The morphological chromosome aberrations detected in the first post-irradiation cell division (dicentrics and centric rings) were studied by Giemsa staining. RESULTS: The chromosome aberrations at 350eV were, respectively, 2.6 +/- 0.8 and 2.1 +/- 0.8 times more numerous than at 250 and 810eV for the same average dose absorbed by the nucleus. These relative effectivenesses are comparable with the ones already measured for cell killing. Moreover, they roughly vary such as the relative numbers of core ionizations (including in the phosphorus L-shell) produced in DNA and its bound water (water being involved only at 810eV through the oxygen atoms). In particular, they reproduce the characteristic twofold enhancement at 350eV, above the carbon K threshold. CONCLUSIONS: Correlations suggest that the core ionization process is likely a common and essential mechanism initiating both chromosome aberration and cell killing end-points at these photon energies.

Animals↗
PubMed1996

Formation of two double-strand breaks in the same DNA molecule by a single high-energy photon or ionizing particle.

I calculate the probability that a single high-energy ionizing particle or photon makes two widely spaced double-strand breaks in the same DNA molecule. Deletions (or inversions) between two breaks formed by the same incident particle are linear in radiation dose and occur even at extremely low dose-rates; deletions between breaks induced by separate particles are quadratic in dose and are much fewer at very low dose-rate. The calculations show that for a few grays of sparsely ionizing radiations such as fast electrons, X-rays of gamma-rays, the formation of two double-strand breaks in a DNA molecule 1 megabase in size should be nearly entirely quadratic in dose. For heavily ionizing particles such as alpha particles from radon products, the linear and quadratic terms are comparable in size. These conclusions are robust and insensitive to details of the calculations. The results are essentially the same for DNA in a random coil configuration and for DNA uniformly and randomly distributed within a sphere.

Chromosome Inversion↗
PubMed1996

Induction of inositol 1,4,5 trisphosphate receptor genes by ionizing radiation.

We used differential display, a method designed to amplify partial cDNA sequences from subsets of mRNAs, to identify mRNAs induced by ionizing radiation in human Epstein Barr Virus (EBV)-transformed lymphoblastoid cells. Increased expression of a cDNA corresponding to the inositol 1,4,5 trisphosphate receptor (InsP3R) type 1 was observed after exposure of cells to 3Gy gamma-rays. This was confirmed by Northern blot analysis. The increase in mRNA for InsP3R type 1 was accompanied by a corresponding increase in the level of InsP3R type 1 protein as determined by Western blotting. Exposure of cells from patients with the human genetic disorder ataxia-telangiectasia (A-T), characterized by hypersensitivity to ionizing radiation, failed to change the levels of InsP3R type 1 mRNA and, as expected, there was no increase in InsP3R type 1 protein in A-T cells in response to radiation exposure. Protein levels for two other InsP3Rs, types 2 and 3, were observed to increase in control and A-T cells after exposure to ionizing radiation. The induction of the InsP3R type 1, which is primarily located in the endoplasmic reticulum, may play an important role in radiation signal transduction.

Base Sequence↗
PubMed1998

Recent epidemiological studies on ionizing radiation and childhood cancer in Germany.

PURPOSE: The results from recent epidemiological studies based on the German Childhood Cancer Registry are summarized. MATERIALS AND METHODS: An oecological study covers 16 years' incidence of childhood malignancies in areas surrounding nuclear facilities and in matched control regions. Two population-based case control studies explore potential risk factors of childhood leukaemia in the state of Lower Saxony (1988 93) and in all western states of Germany (1992-94). RESULTS: There was no increased incidence of childhood leukaemia and other malignancies in the vicinity of nuclear installations. X-ray examinations during pregnancy and in early childhood were not associated with an increased risk of childhood leukaemia. There were no data to support Gardner's hypothesis of an increased risk due to paternal pre-conception exposure to ionizing radiation. Following the Chernobyl accident, the reported incidence of neuroblastoma and infant leukaemia was increased. The increase cannot be explained by exposures due to the accident. CONCLUSIONS: Although the carcinogenic effect of ionizing radiation is well known, the recent population-based epidemiological studies show that under current conditions exposure to ionizing radiation in Germany does not constitute risks of childhood malignancies that are relevant to public health.

Case-Control Studies↗
PubMedDate not supplied

Hypoxia and ionizing radiation: changes in adhesive properties and cell adhesion molecule expression in MG-63 three-dimensional tumor spheroids.

The effects of chemically induced hypoxia and ionizing radiation on the adhesive properties of MG-63 human osteosarcoma three-dimensional spheroids were investigated. Hypoxia was induced by addition of CoCl2 to small, nonhypoxic spheroids and verified by HIF-1alpha expression. In addition, the possible role of important cell adhesion molecules involved in tumor dissemination in inducing adhesive changes were also studied. In particular, two key integrins (i.e., the alpha chain of the fibronectin receptor, alpha5, and the alpha chain of the collagen receptor, alpha2), an important member of the immunoglobulin superfamily (CD54 or ICAM-1) and the strategic molecule CD44 (H-CAM, the principal receptor for hyaluronan) were examined. Because of the important role of fibronectin in adhesive processes, variations in this extracellular matrix component were also examined. The results seem to indicate that CoCl2-induced hypoxia greatly increases adhesion of MG-63 spheroids to both tissue culture plates and plates coated with fibronectin or collagen when compared to controls, while ionizing radiation induces a great decrease in this attachment. Furthermore, chemically induced hypoxia also partially inhibits the effects of ionizing radiation. The data also show that these adhesive changes are accompanied by concomitant variations in the expression of alpha5 and alpha2 integrins, CD44, and CD54 and fibronectin.

Adhesiveness↗
PubMed1994

Ionizing radiation acts on cellular membranes to generate ceramide and initiate apoptosis.

Recent investigations provided evidence that the sphingomyelin signal transduction pathway mediates apoptosis for tumor necrosis factor alpha (TNF-alpha) in several hematopoietic and nonhematopoietic cells. In this pathway, TNF-receptor interaction initiates sphingomyelin hydrolysis to ceramide by a sphingomyelinase. Ceramide acts as a second messenger stimulating a ceramide-activated serine/threonine protein kinase. The present studies show that ionizing radiation, like TNF, induces rapid sphingomyelin hydrolysis to ceramide and apoptosis in bovine aortic endothelial cells. Elevation of ceramide with exogenous ceramide analogues was sufficient for induction of apoptosis. Protein kinase C activation blocked both radiation-induced sphingomyelin hydrolysis and apoptosis, and apoptosis was restored by ceramide analogues added exogenously. Ionizing radiation acted directly on membrane preparations devoid of nuclei, stimulating sphingomyelin hydrolysis enzymatically through a neutral sphingomyelinase. These studies provide the first conclusive evidence that apoptotic signaling can be generated by interaction of ionizing radiation with cellular membranes and suggest an alternative to the hypothesis that direct DNA damage mediates radiation-induced cell kill.

Animals↗
PubMed2005

Efficient inhibition of human telomerase reverse transcriptase expression by RNA interference sensitizes cancer cells to ionizing radiation and chemotherapy.

Telomerase activation plays critical roles in tumor growth and progression in part through the maintenance of telomere structure. Indeed, the ubiquitous expression of telomerase in human cancers makes telomerase a promising target for cancer therapy. Genetic, pharmacologic, and antisense methods to inhibit telomerase have been described; however, in most cases, cancer cell death was observed only after many cell divisions. Here, using retroviral delivery of small interfering RNAs (siRNAs) specific for the human telomerase reverse transcriptase (hTERT), we successfully inhibited telomerase activity in cervical cancer cell lines. Cells lacking hTERT expression exhibited significantly decreased telomerase activity and showed shortened telomeres and telomeric 3' overhangs with passage. These cells entered replicative senescence after a considerable number of cell divisions. Notably, the proliferative rate of these cells was significantly impaired, compared with control cells with telomerase activity, even in low-passage cells (population doubling 5). Likewise, colony-forming ability and tumorigenicity in mice were attenuated in low-passage cells lacking hTERT. We further examined the effects of chemotherapy and ionizing radiation on cells in which hTERT expression was suppressed. Cells lacking hTERT showed a significantly increased sensitivity, compared with control cells, to ionizing radiation or chemotherapeutic agents that induce DNA double- strand breaks, such as topoisomerase inhibitors or bleomycin. These findings suggest that an siRNA-based strategy can be applied to the development of novel telomerase inhibitors, the antitumor effects of which may be enhanced in combination with ionizing radiation and chemotherapy.

Animals↗
PubMed2002

Micronuclei frequencies in hospital workers occupationally exposed to low levels of ionizing radiation: influence of smoking status and other factors.

In the context of a medical surveillance program aimed at preventing cancer risk from exposure to ionizing radiation, we investigated chromosomal damage in peripheral lymphocytes from 37 hospital workers exposed to low levels of ionizing radiation and 37 controls. The micronuleus (MN) assay was used as a biomarker of genetic damage. The influence of confounding factors like smoking status, age and gender was investigated by multiple regression analysis. The results indicated that, overall, MN frequency was higher in exposed workers than in controls, although the difference was not statistically significant. Interestingly, smoking status significantly raised MN frequency among the exposed workers but not among controls. This suggests that smoking can influence chromosomal damage induced in humans by ionizing radiation. Among both exposed workers and controls, MN frequency was found to increase with age. Female gender influenced the increase in MN frequency in the exposed group. Our results suggest that the effect of cigarette smoking should be carefully factored into genetic monitoring studies assessing the risks associated with low level radiation exposure.

Adult↗
PubMed2003

The alkaline Comet assay as biomarker in assessment of DNA damage in medical personnel occupationally exposed to ionizing radiation.

The alkaline Comet assay was selected as a biomarker of exposure to evaluate the ongoing exposure to ionizing radiation of 50 medical workers occupationally exposed to ionizing radiation and 50 corresponding unexposed control subjects. The primary DNA damage was evaluated by measuring the extent of DNA migration in peripheral blood leukocytes. The inter-individual differences in DNA damage between exposed subjects were compared with their dosimeter readings and occupation. It was found that medical workers who were occupationally exposed to ionizing radiation for different periods of time showed highly significant increases in levels of DNA damage compared with controls. However, influences of the different occupational settings and doses absorbed on the levels of DNA damage, assessed by use of the Comet assay, might be excluded in the majority of subjects. Differences in comet parameters measured due to smoking and gender were not statistically significant in either exposed or control subjects. The results obtained have confirmed the usefulness of the alkaline Comet assay as an additional complement to standard biodosimetric methods. By detection of momentary DNA damage and/or repair activity, it reflects the concurrent exposure and the actual levels of DNA damage present in peripheral blood leukocytes of the radiological workers at the moment of blood sampling.

Biomarkers↗
PubMed1994

Mortality through 1990 among white male workers at the Los Alamos National Laboratory: considering exposures to plutonium and external ionizing radiation.

A cohort mortality study was conducted of 15,727 white men employed by the Los Alamos National Laboratory, a nuclear research and development facility. Some of the workers at this facility have been exposed to various forms of ionizing radiation and other potentially hazardous materials. These analyses focused on whole-body ionizing radiation exposures and internal depositions of plutonium. The results indicated that overall mortality among this cohort is quite low, even after nearly 30 y of follow-up. No cause of death was significantly elevated among plutonium-exposed workers when compared with their unexposed coworkers; however, a rate ratio for lung cancer of 1.78 (95% CI = 0.79-3.99) was observed. A case of osteogenic sarcoma, a type of cancer related to plutonium exposure in animal studies, was also observed. Dose-response relationships for whole-body dose from external ionizing radiation and tritium were observed for cancers of the brain/central nervous system, the esophagus, and Hodgkin's disease.

Cohort Studies↗
PubMed1984

Ionizing radiation for treatment of benign conditions.

Ionizing radiation has been used much more frequently in the past than at the present in the treatment of benign conditions. As progress continued in the medical sciences, the use of radiotherapy narrowed considerably due to better understanding of the nature of ionizing radiation and its potential complications. Other agents have replaced ionizing radiation in some areas, but there are still conditions that benefit from this treatment. This article reviews the basic principles that should be observed in treating benign conditions with radiotherapy.

Humans↗
PubMed1992

No adaptive response of Chinese hamster ovary cells to low doses of ionizing radiation.

Chinese hamster ovary (CHO) cells that had been exposed to very low doses of ionizing radiation from incorporated tritiated thymidine or X-rays were shown not to be more resistant to the induction of chromatid aberrations by a subsequent higher dose of ionizing radiation than previously untreated cells. The adaptive response to ionizing radiation was absent both in cells challenged with high doses of X-rays (1.25 Gy) and in cells post-treated with thermal neutrons (0.5-1 x 10(12) n/cm2). In agreement with these observations in CHO cells we were unable to demonstrate an adaptive response to X-rays also in human lymphocytes from five different donors.

Adaptation, Physiological↗
PubMedDate not supplied

A review of the processes by which ultrasound is generated through the interaction of ionizing radiation and irradiated materials: some possible applications.

The production of acoustic waves following the absorption of energy deposited by ionizing radiation, with a consequent production of localized thermal spikes has been confirmed by a number of papers published in the physics literature. This paper reviews the basic theory and presents most of the supporting experimental data. Some of the experimental methods used and the results obtained are summarized. In addition to the rather straightforward and routine use of acoustic phenomena produced by ionizing radiation for the detection and measurements of such radiation, there are some special applications that appear to be especially attractive for medical physics. Some of these are unique to ionizing radiation in that the amplitude of the ultrasound wave is proportional to the energy deposited in small volumes at localized sites of these interactions, while others derive from methodologies already in use with nonionizing radiations. The detection and measurement of this ultrasonic radiation could possibly lead to methods for the study of such fundamental phenomenon as track structure, precision localization of therapeutic treatment beams, and even the possible imaging of internal anatomic structures to provide on-line portal images.

Hot Temperature↗
PubMed1998

Activation of the ATM kinase by ionizing radiation and phosphorylation of p53.

The p53 tumor suppressor protein is activated and phosphorylated on serine-15 in response to various DNA damaging agents. The gene product mutated in ataxia telangiectasia, ATM, acts upstream of p53 in a signal transduction pathway initiated by ionizing radiation. Immunoprecipitated ATM had intrinsic protein kinase activity and phosphorylated p53 on serine-15 in a manganese-dependent manner. Ionizing radiation, but not ultraviolet radiation, rapidly enhanced this p53-directed kinase activity of endogenous ATM. These observations, along with the fact that phosphorylation of p53 on serine-15 in response to ionizing radiation is reduced in ataxia telangiectasia cells, suggest that ATM is a protein kinase that phosphorylates p53 in vivo.

Ataxia Telangiectasia Mutated Proteins↗