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Results for “Radiation, Ionizing”

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PubMedDate not supplied

[Bone marrow hemopoiesis at emotional stress reactions of various intensity upon a background of exposure to low dose ionizing radiation].

Rats preliminary exposed to 0.9 Gy of ionizing radiation showed disturbances in the development of adaptive reactions of blood system to emotional stress, compensatory capacity of the blood system being decreased. A degree of the disturbances directly depended on the duration and intensity of the emotional stress: at the prolonged intensive emotional stress a sharp decrease in the adaptive and compensatory capacity of blood system was found; at short intensive or moderate stress the changes in the adaptive and compensatory capacity of hemopoiesis were less pronounced. A combined action of low-dose ionizing radiation and short weak emotional stress did non affect the adaptive and compensatory capacity of hemopoietic system.

Adaptation, Physiological↗

PubMed1996

Infrequent alterations of the p53 gene in rat skin cancers induced by ionizing radiation.

Radiation carcinogenesis almost certainly involves multiple genetic alterations. Identification of such genetic alterations would provide information to help understand better the molecular mechanism of radiation carcinogenesis. The energy released by ionizing radiation has the potential to produce DNA strand breaks, major gene deletions or rearrangements, and other base damages. Alterations of the p53 gene, a common tumour suppressor gene altered in human cancers, were examined in radiation-induced rat skin cancers. Genomic DNA from a total of 33 rat skin cancers induced by ionizing radiation was examined by Southern blot hybridization for abnormal restriction fragment patterns in the p53 gene. An abnormal p53 restriction pattern was found in one of 16 cancers induced by electron radiation and in one of nine cancers induced by neon ions. The genomic DNA from representative cancers, including the two with an abnormal restriction pattern, was further examined by polymerase chain reaction amplification and direct sequencing in exons 5-8 of the p53 gene. The results showed that one restriction fragment length polymorphism (RFLP)-positive cancer induced by electron radiation had a partial gene deletion which was defined approximately between exons 2-8, while none of the other cancers showed sequence changes. Our results indicate that the alterations in the critical binding region of the p53 gene are infrequent in rat skin cancers induced by either electron or neon ion radiation.

Animals↗

PubMed1990

Ionizing radiation regulates expression of the c-jun protooncogene.

There is little known about the regulation of gene expression by ionizing radiation exposure. The present studies demonstrate transcriptional activation of a mammalian gene, the c-jun protooncogene, by x-rays. The c-jun gene encodes a component of the AP-1 protein complex and is important in early signaling events involved in various cellular functions. The increase in c-jun transcripts by ionizing radiation was time- and dose-dependent as determined by Northern blot analysis. Transcriptional run-on analysis demonstrated that ionizing radiation stimulates the rate of c-jun gene transcription. Furthermore, the half-life of c-jun RNA was prolonged in the absence of protein synthesis. These findings indicate that the increase in c-jun RNA observed after irradiation is regulated by transcriptional and posttranscriptional mechanisms. Moreover, the induction of c-jun by ionizing radiation was associated with an inverse dose rate effect in that decreasing the dose rate resulted in increased c-jun expression. The present results similarly demonstrate that ionizing radiation increases levels of c-fos transcripts as well as that of jun-B, another member of the jun family. Taken together, these results suggest a role for induction of early response genes in the pathophysiologic effects of ionizing radiation.

Blotting, Northern↗

PubMed1994

Ionizing radiation induces rapid tyrosine phosphorylation of p34cdc2.

Eukaryotic cells respond to ionizing radiation exposure with cell cycle arrest. However, little is known about the signaling mechanisms responsible for this effect. The present work has asked whether ionizing radiation exposure is associated with changes in phosphorylation of proteins in HL-60 myeloid leukemia cells. The results demonstrate increased tyrosine phosphorylation of a M(r) 34,000 substrate. This effect was detectable at 1 to 10 min after irradiation and was induced by doses of 50 to 500 cGy. Immunoprecipitation studies further suggest that this substrate is the serine/threonine p34cdc2 protein kinase. Since p34cdc2 is required for entry into mitosis, these findings support the posttranslational modification of a cell cycle regulatory protein in the response to ionizing radiation.

CDC2 Protein Kinase↗

PubMed1990

Effects of ionizing radiation on the blood brain barrier permeability to pharmacologically active substances.

Ionizing radiation can impair the integrity of the blood brain barrier (BBB). Data on early and late damage after brain irradiation are usually reported separately, yet a gradual transition between these two types has become evident. Signs appearing within 3 weeks after irradiation are considered to be early manifestations. The mechanism of radiation-effected integrity impairment of the BBB is discussed in relation to changes in morphological structures forming the BBB, the endothelium of intracerebral vessels, and in the surrounding astrocytes. Alterations in the function of the BBB are manifested in the endothelium by changes in the ultra-structural location of the activity of phosphatases and by the activation of pinocytotic vesicular transport, and in astrocyte cytoplasm by glycogen deposition. The changes in ultrastructure were critically surveyed with regard to increasing doses of radiation to the brain in the range of 5 Gy to 960 Gy. The qualitative as well as the semiquantitative and quantitative observations on the passage of substances across the damaged BBB were treated separately. Qualitative changes are based mainly on findings of extravasation of vital stains and of labelled proteins. The quantitative studies established differences in radiation-induced changes in the permeability of the BBB depending on the structure and physico-chemical properties of the barrier penetrating tracers. Indirect evaluation of radiation-induced BBB changes is based on studies of pharmacological effects of substances acting on the CNS. In conclusion, radiation impairs significantly the integrity of the BBB following single irradiation of the brain with a dose exceeding 10-15 Gy. The response of the BBB to ionizing radiation is dependent both on the dose to which the brain is exposed and on specific properties of the tracer. Either an increase or a decrease of BBB permeability, or both, occurring in a certain time sequence, was observed. The mechanism of hyperpermeability after irradiation is not fully understood, but the activation of vesicular transport offers one possible explanation. Even less understood is the mechanism of decreased permeability. The response of the BBB to ionizing radiation is most probably nonspecific and its nature may be assumed to be similar to its responses to other physical or chemical noxious factors.

Blood-Brain Barrier↗

PubMed2000

Mitogen-activated protein kinase, ERK1/2, is essential for the induction of vascular endothelial growth factor by ionizing radiation mediated by activator protein-1 in human glioblastoma cells.

Vascular Endothelial Growth Factor (VEGF)/Vascular Permeability Factor plays an important role in angiogenesis and cell proliferation of cancer cells. Glioblastoma cells are most malignant and show resistance to radiation therapy inducing VEGF to cause angiogenesis and brain edema. In the present study, the regulatory mechanism of the expression of VEGF by ionizing radiation was studied in three human glioblastoma cells. Induction of VEGF mRNA by ionizing radiation was dependent on dose and incubation time. Activator protein-1 (AP-1) was activated by 10 Gy of ionizing radiation in 1 h in T98G glioblastoma cells on an electrophoretic mobility shift assay. We constructed chimeric genes containing various regions of the VEGF promoter gene and the coding region for chloramphenicol acetyltransferase (CAT) and transiently transfected them to T98G cells. CAT assay with the VEGF promoter gene containing an AP-1 site demonstrated that the promoter activity of the VEGF gene was enhanced by ionizing radiation. Immunological analysis of the activity of mitogen-activated protein kinase, ERK1/2, showed that this activity is up-regulated by ionizing radiation. These results suggest that ERK1/2 pathway is involved in the up-regulation of VEGF expression ionizing radiation mediated by AP-1, which may lead to further neovascularization and proliferation of glioblastoma cells resistant to radiation therapy.

Blotting, Northern↗

PubMed2004

Ionizing radiation induces delayed hyperrecombination in Mammalian cells.

Exposure to ionizing radiation can result in delayed effects that can be detected in the progeny of an irradiated cell multiple generations after the initial exposure. These effects are described under the rubric of radiation-induced genomic instability and encompass multiple genotoxic endpoints. We have developed a green fluorescence protein (GFP)-based assay and demonstrated that ionizing radiation induces genomic instability in human RKO-derived cells and in human hamster hybrid GM10115 cells, manifested as increased homologous recombination (HR). Up to 10% of cells cultured after irradiation produce mixed GFP(+/-) colonies indicative of delayed HR or, in the case of RKO-derived cells, mutation and deletion. Consistent with prior studies, delayed chromosomal instability correlated with delayed reproductive cell death. In contrast, cells displaying delayed HR showed no evidence of delayed reproductive cell death, and there was no correlation between delayed chromosomal instability and delayed HR, indicating that these forms of genome instability arise by distinct mechanisms. Because delayed hyperrecombination can be induced at doses of ionizing radiation that are not associated with significantly reduced cell viability, these data may have important implications for assessment of radiation risk and understanding the mechanisms of radiation carcinogenesis.

Chromosomal Instability↗

PubMed1990

Health effects of ionizing radiation.

Although humans have evolved in an environment of ionizing radiation, it was not until man-made sources were developed that the effects of ionizing radiation started to become known. Detection and measurement of radiation is not only sophisticated but widely applied. This article deals with exposure to this kind of radiation and the risk it may cause.

Accidents↗

PubMed2005

Extensive diversity of ionizing-radiation-resistant bacteria recovered from Sonoran Desert soil and description of nine new species of the genus Deinococcus obtained from a single soil sample.

The ionizing-radiation-resistant fractions of two soil bacterial communities were investigated by exposing an arid soil from the Sonoran Desert and a nonarid soil from a Louisiana forest to various doses of ionizing radiation using a (60)Co source. The numbers of surviving bacteria decreased as the dose of gamma radiation to which the soils were exposed increased. Bacterial isolates surviving doses of 30 kGy were recovered from the Sonoran Desert soil, while no isolates were recovered from the nonarid forest soil after exposure to doses greater than 13 kGy. The phylogenetic diversities of the surviving culturable bacteria were compared for the two soils using 16S rRNA gene sequence analysis. In addition to a bacterial population that was more resistant to higher doses of ionizing radiation, the diversity of the isolates was greater in the arid soil. The taxonomic diversity of the isolates recovered was found to decrease as the level of ionizing-radiation exposure increased. Bacterial isolates of the genera Deinococcus, Geodermatophilus, and Hymenobacter were still recovered from the arid soil after exposure to doses of 17 to 30 kGy. The recovery of large numbers of extremely ionizing-radiation-resistant bacteria from an arid soil and not from a nonarid soil provides further ecological support for the hypothesis that the ionizing-radiation resistance phenotype is a consequence of the evolution of other DNA repair systems that protect cells against commonly encountered environmental stressors, such as desiccation. The diverse group of bacterial strains isolated from the arid soil sample included 60 Deinococcus strains, the characterization of which revealed nine novel species of this genus.

DNA, Bacterial↗

PubMed1997

Biodosimetry of ionizing radiation by selective painting of prematurely condensed chromosomes in human lymphocytes.

Painting of interphase chromosomes can be useful for biodosimetric purposes in particular cases such as radiation therapy, accidental exposure to very high radiation doses and exposure to densely ionizing radiation, for example during space missions. Biodosimetry of charged-particle radiation is analyzed in the present paper. Target cells were human peripheral blood lymphocytes irradiated in vitro with gamma rays, protons and iron ions. After exposure, lymphocytes were incubated for different times to allow repair of radiation-induced damage and then fused to mitotic hamster cells to promote premature condensation in the interphase chromosomes. Chromosome spreads were then hybridized with whole-chromosome DNA probes labeled with fluorescent stains. Dose-response curves for the induction of chromatin fragments shortly after exposure, as well as the kinetics of rejoining and misrejoining, were not markedly dependent on linear energy transfer. However, after exposure to heavy ions, more aberrations were scored in the interphase cells after incubation for repair than in metaphase samples harvested at the first postirradiation mitosis. On the other hand, no significant differences were observed in the two samples after exposure to sparsely ionizing radiation. These results suggest that interphase chromosome painting can be a useful tool for biodosimetry of particle radiation.

Animals↗

PubMed2006

Quantitative analysis reveals asynchronous and more than DSB-associated histone H2AX phosphorylation after exposure to ionizing radiation.

Rapid phosphorylation of histone H2AX after exposure of cells to ionizing radiation occurs at DSB sites and extends to a region including as much as 30 Mbp of chromatin to form visible microscopic structures called gamma-H2AX foci. Although the kinetics of total cellular histone H2AX phosphorylation after irradiation has been characterized, we still know little about the phosphorylation kinetics of individual gamma-H2AX foci. In addition, there are hundreds of smaller gamma-H2AX foci that are not associated with DNA double-strand breaks. We refer to these sites as DSB-unrelated gamma-H2AX foci. By using indirect immunofluorescence microscopy, deconvolution and three-dimensional image analysis, we established an objective method to quantitatively analyze each gamma-H2AX focus as well as to discriminate DSB-related gamma-H2AX foci from DSB-unrelated gamma-H2AX foci. Using this method, we found that histone H2AX phosphorylation at different DSB sites was asynchronous after exposure to ionizing radiation. This may reflect the heterogeneous characteristic of free DNA ends that are generated under these conditions. In addition, we found that increased histone H2AX phosphorylation also occurred outside of DSB sites after exposure to ionizing radiation. The function of this DSB-unassociated phosphorylation is not known.

Cell Line, Tumor↗

PubMed2006

Ionizing radiation synergistic induction of cyclooxygenase-2 with benzo[a]pyrene diol-epoxide through nuclear factor of activated T cells in mouse epidermal Cl 41 cells.

Carcinogenic effects of ionizing radiation and benzo[a]pyrene-7,8-diol-9,10-epoxide (B[a]PDE), a major metabolite of benzo[a]pyrene (B[a]P), have been well demonstrated both in vitro and in vivo. Two-stage carcinogenesis results indicate that mouse skin is highly susceptible to both ionizing radiation and benzo[a]pyrene-7,8-diol-9,10-epoxide (B[a]PDE), a major metabolite of benzo[a]pyrene (B[a]P). It is believed that signaling pathways leading to the regulation of gene expression play a significant role in the development of skin cancers. The NFAT family of proteins are important transcription factors involved in the regulation of various target genes, such as IL-1 and TNF-alpha, which play key roles in the regulation of inflammation and carcinogenesis. Thus, the effect of ionizing radiation and B[a]PDE on COX-2 induction and NFAT3 activation, and their relationship, was investigated in mouse epidermal Cl 41 cells. We found that B[a]PDE exposure induced a very high level of NFAT activation in mouse epidermal Cl 41 cells. Ionizing radiation exhibited a synergistic effect with B[a]PDE on NFAT activation and COX-2 induction, while ionizing radiation alone had no effect. By stably knocking down NFAT3 protein expression by means of the specific interfering RNA (siRNA) technique, we found that COX-2 induction by B[a]PDE and the synergistic effect of ionizing radiation with B[a]PDE was totally blocked. These results indicate that ionizing radiation acts synergistically with B[a]PDE on COX-2 induction, and the synergism is dependent on the NFAT3 pathway.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed2006

Biological dosimetry -- cytogenetics findings at persons occupationally exposed to ionizing radiation.

A large number of physical and chemical agents are capable to course chromosomal aberrations. Ionizing radiation is frequent and well known course of chromosomal aberrations. If deoxyribonucleic acid (DNA) is irradiated before synthesis chromosomal-type aberrations are caused. Chromatid-type aberrations are results of DNA damages occurred during or after synthesis. Some of these changes could exist at patients several years after exposition. Biological dosimetry-cytogenetics analysis of persons occupational exposed to ionizing radiation in Federation of Bosnia and Herzegovina have been carried out in "Center for Human Genetics" of Medical Faculty in Sarajevo. In this study we have evaluated cytogenetics findings of persons employed in a zone of radiation. Cytogenetics findings have been demonstrated in allowed limit in 154 (81.1%) examinees, and cytogenetics findings were out of normal values in 36 (18.9%) examinees. The majorities who have been employed in a zone of ionizing radiation were in age group 40-44 (25.3%) and age group 45-49 (24.7%). Radiological technicians (35.7%) were exposed the most to ionizing radiation, than clinical nurse specialists (14.7%), radiologists (11.1), physicians (7.4%) machines technicians (6.3%), pneumologists (4.7%), orthopedists (4.2%) and scrub nurses (4.2%). Biological dosimetry-cytogenetics analysis have been carried out at 108 (56.8%) male and 82 (43.2%) female examinees. The most frequent aberration have been presented with 26.8% in the form of acentric fragments, than chromatid fragments with 21.2%, dicentric chromosomes with 19.5%, gaps with 18.7%, minutes with 12.2% and inter-arm interchanges with 1.6%.

Adult↗

PubMed1986

Ionizing radiation promotes protozoan reproduction.

This experiment was performed to determine whether ionizing radiation is essential for maximum growth rate in a ciliated protozoan. When extraneous ionizing radiation was reduced to 0.15 mrad/day, the reproduction rate of Tetrahymena pyriformis was significantly less (P less than 0.01) than it was at near ambient levels, 0.5 or 1.8 mrad/day. Significantly higher growth rates (P less than 0.01) were obtained when chronic radiation was increased. The data suggest that ionizing radiation is essential for optimum reproduction rate in this organism.

Background Radiation↗

PubMed1977

Infrared spectral characterization of peptidic material produced by ionizing radiation in aqueous cyanides.

Oligomers formed by ionizing radiation in aqueous cyanide solutions, under various experimental conditions, have been characterized by infrared spectroscopy. IR bands appear in the region known to be characteristic for amides and peptides. The results are discussed in relation to radiation-induced formation of peptidic material and the potential role of ionizing radiation as an energy source for some processes in prebiotic molecular evolution.

Cyanides↗

PubMed1996

The effect of ionizing radiation on signal transduction: antibodies to EGF receptor sensitize A431 cells to radiation.

What determines the degree of cell-resistance or sensitivity to ionizing radiation is not yet known. As a corollary to the ability of ceramide to induce apoptosis, some questions arise as to whether malignant cells escape apoptosis because of their inability to mount a ceramide response to inducers of apoptosis. To shed more light on the molecular mechanisms of tumor cell response to radiation, we tested whether exposure to ionizing radiation (of 200-1000 cGy) is associated with changes in ceramide levels in A431 tumor epithelial cells and whether the ability of ceramide to induce apoptosis is inhibited by protein kinase C (PKC) activation. Our studies demonstrate an immediate decrease in cellular levels of ceramide in response to radiation, while sphingosine levels increase. Under the same conditions the cellular 1,2-diacylglycerol (DAG) levels decrease as well, being accompanied by the translocation of PKC alpha from the membrane to the cytoplasm. Elevation of membrane PKC levels by 12-O-tetradecanoylphorbol 13-acetate (TPA) treatment had no effect on cell survival after irradiation, while treatment with EGF during and after irradiation augmented cell survival. Moreover, monoclonal antibodies to the EGF receptor (EGFR) sensitize cells to radiation by facilitating radiation-induced apoptosis. It is thus plausible that in human Squamous carcinoma cells, radiation activates predominantly the EGFR to induce resistance, while both sphingomyelin and PKC signal transduction pathways are deactivated and demonstrate no significant role in the modulation of the sensitivity or the resistance of A431 cells to ionizing radiation.

Antibodies↗

PubMed1997

Mathematical description of synergistic interaction of hyperthermia and ionizing radiation.

A simple mathematical model of simultaneous combined action of ionizing radiation and hyperthermia has been proposed. The model suggests that the synergistic interaction of ionizing radiation and hyperthermia is expected to result from the additional lethal damage arising from the interaction of sublesions induced by both agents. These sublesions are considered nonlethal after each agent taken alone. The model was applied to the quantitative analysis of the simultaneous action of hyperthermia and ionizing radiation. It predicts the dependence of synergistic interaction of the ratio of lethal events produced by every agent used, as well as the maximal value of the synergistic effect, conditions at which the maximal interactive effect can be achieved, and the dependence of synergistic effect on dose rate. The predictions of the model have been tested with four experimental data sets reported in the literature. The theory appears to be appropriate and the conclusions valid.

Animals↗

PubMed2002

Effects of combined photodynamic therapy and ionizing radiation on human glioma spheroids.

The effects of combined photodynamic therapy (PDT) and ionizing radiation are studied in a human glioma spheroid model. The degree of interaction between the two modalities depends in a complex manner on factors such as PDT irradiation fluence, fluence rate and dose of ionizing radiation. It is shown that gamma radiation and PDT interact in a synergistic manner only if both light fluence and gamma radiation dose exceed approximately 25 J cm(-2) and 8 Gy, respectively. Synergistic interactions are observed only for the lower fluence rate (25 mW cm(-2)) investigated. The degree of interaction appears to be independent of both sequence and the PDT or ionizing radiation time intervals investigated (1 and 24 h). Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assays show that low-fluence rate PDT is very efficient at inducing apoptotic cell death, whereas neither high-fluence rate PDT nor ionizing radiation produces significant apoptosis. Although the mechanisms remain to be elucidated, the data imply that the observed synergism is likely not due to gamma-induced cell cycle arrest or to PDT-induced inhibition of DNA repair.

Brain Neoplasms↗