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Results for “Radiation, Ionizing”

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PubMed1998

Role of antioxidant enzymes on ionizing radiation resistance.

Exposure of cells to ionizing radiation leads to formation of reactive oxygen species (ROS) that are associated with radiation-induced cytotoxicity. The antioxidant enzymes manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD), and glutathione peroxidase (GPx), are key intracellular antioxidants in the metabolism of ROS. We investigated the potential role of the three antioxidant enzymes in radioresistance by analyzing cell morphology, cell viability, and cellular radioresistance in stably transfected CHO cell lines overexpressing MnSOD, CuZnSOD, and GPx, respectively. We found that overexpression of human MnSOD substantially protected cells from ionizing radiation injury. Relative to MnSOD, GPx could slightly reduce the radiation sensitivity while the radioresistance in CuZnSOD expressing cells did not change significantly. The results suggested that MnSOD may play a central role in protecting cells against reactive oxygen species injury during ionizing radiation exposure among MnSOD, CuZnSOD, and GPx.

Animals↗

PubMed1996

Vascular effects of occupational exposure to low-dose ionizing radiation.

Damage to the microcirculation caused by high-dose ionizing radiation is well known but data concerning low-dose exposure are scant and contrasting. We employed capillary microscopy to study dermal microcirculation damage resulting from occupational exposure to ionizing radiation doses lower than 5 rem/year (maximum permissible dose in Italy). We studied 145 physicians (60.7% radiologists, 33.8% orthopedic specialists, 5.5% cardiologists) occupationally exposed to ionizing radiation and a control group of 106 subjects in comparable but different occupations not exposed to ionizing radiation or to other skin hazards. All subjects were administered a clinical protocol and underwent capillary microscopy of the fingernail-fold. Capillary microscopy alterations were classified as absent, mild, moderate, marked and severe. Our data confirm that occupational exposure to low-dose ionizing radiation can lead to morphological and functional alterations of the dermal microcirculation, which can be identified early by capillary microscopy.

Adult↗

PubMed1995

Modification of nucleolar protein B23 after exposure to ionizing radiation.

The responses of cells to ionizing radiation include induction and/or suppression of the expression of genes and proteins. In our investigations of alterations in cellular protein expression in response to ionizing radiation, we have used the techniques of two-dimensional polyacrylamide gel electrophoresis and silver staining. We compared the nuclear protein profiles of control and irradiated (6 Gy, 4 h postirradiation) radioresistant squamous carcinoma cells (SQ-20B) and observed an alteration in the expression of a 40 kDa protein: control nuclei express a protein isoform with pI values between 5.4-5.8, while irradiated nuclei express a more acidic variant with pI values between 5.2-5.5. Using the cyanogen bromide/O-phthalaldehyde method followed by microsequencing analysis, we obtained an internal amino acid sequence and identified the 40 kDa protein as nucleolar protein B23. Western blotting experiments confirmed the internal amino acid sequencing results and showed both species (control, 5.4-5.8, irradiated, 5.2-5.5) to be recognized by an anti-B23 monoclonal antibody. Radiolabeling of control and irradiated samples with [32P]NAD or [32P]orthophosphoric acid revealed the acidic species of B23 to be both ADP-ribosylated and phosphorylated. Therefore, exposure of SQ-20B cells to radiation results in the increase in expression of an ADP-ribosylated and phosphorylated species of B23.

Adenosine Diphosphate Ribose↗

PubMed2002

Degradation of 2,4-dichlorophenoxyacetic acid by ionizing radiation: influence of oxygen concentration.

Ionizing radiation has been proved as a promising method for the degradation of the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D). The gamma-radiolytic decomposition and chloride formation follows an apparent first order kinetic, kde/kCl = 3. For complete removal of 500 microM 2,4-D, a dose of 4 kGy is required. Phenolic intermediates (2,4-dichlorophenol, the isomers 2-chloro-4-hydroxy- and 4-chloro-2-hydroxy phenoxyacetic acid and three hydroxylation products of 2,4-D) are formed. Using oxygen saturation during irradiation, they are removed again with a dose of 4 kGy. For the formation of the main organic product acetic acid a reaction mechanism is discussed. Oxygen concentration enhances strongly fragmentation and mineralization. A reduction of 36% TOC could be achieved.

2,4-Dichlorophenoxyacetic Acid↗

PubMed1993

Postnatal development of the rat CNS following in utero exposure to a low dose of ionizing radiation.

In utero exposure to ionizing radiation is of importance because of its potential health risks. The developing nervous system is particularly vulnerable and the consequences of exposure to low levels of radiation (< or = 1 Gy) are not well established. The developmental effects of maternal exposure to 50 cGy gamma-radiation on gestational days (GD) 9.5, 15, and 18 were investigated in Sprague Dawley rats. Rats exposed on GD-9.5 along with appropriate controls were killed at 4 h, 48 h, and 10 days post-irradiation while those irradiated on GD-15 and GD-18 were killed postnatally (PN) on days 7 and 26. All were examined for developmental anomalies and representative samples of brains were processed for microscopic study. No significant developmental differences were observed between irradiated and control embryos killed 48 h after irradiation on GD 9.5. However, in irradiated fetuses a larger number of developmental anomalies were observed at term. Defects of the eye and of spinal curvature were the most common malformations encountered. Mitoses were reduced within the neuroepithelium of embryos irradiated on GD-9.5 and evidence of pyknosis and necrosis was seen 4 h after irradiation. The capacity of surviving primitive neural cells for repair, however, was such that by 48 h after exposure the irradiated nervous system no longer differed from controls. Rats irradiated on GD-15 and GD-18 and examined on PN-26 exhibited clusters of small, dark, pyknotic neurons within the hippocampal and dentate gyri, often bilaterally.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Radiation-Induced↗

PubMed1994

Activation of the pp90rsk and mitogen-activated serine/threonine protein kinases by ionizing radiation.

The cellular response to ionizing radiation (IR) includes induction of the c-jun and EGR1 early response genes. The present work has examined potential cytoplasmic signaling cascades that transduce IR-induced signals to the nucleus. The results demonstrate activation of the 40S ribosomal protein S6 kinase, pp90rsk, in human U-937 myeloid leukemia cells. Partial purification of pp90rsk by affinity chromatography demonstrated an increase in S6 peptide phosphorylation when comparing irradiated with control cells. IR-induced activation of pp90rsk was further confirmed in immune-complex kinase assays. In contrast to these findings, there was no detectable induction of pp70S6K. Previous work has demonstrated that mitogen-activated protein kinase activates pp90rsk. The present results further show that IR treatment is associated with induction of mitogen-activated protein kinase activity and that this event is temporally related to activation of pp90rsk and early response gene expression. These findings suggest that activation of the mitogen-activated protein kinase/pp90rsk cascade is involved in the response of cells to IR exposure.

Base Sequence↗

PubMed2003

Novel localization of the DNA-PK complex in lipid rafts: a putative role in the signal transduction pathway of the ionizing radiation response.

Increased sensitivity to ionizing radiation (IR) has been shown to be due to defects in DNA double-strand break repair machinery. The major pathway in mammalian cells dedicated to the repair of DNA double-strand breaks is by the nonhomologous end-joining machinery. Six components function in this pathway, of which three (Ku70, Ku86, and DNA-PKcs) constitute a protein complex known as DNA-dependent protein kinase (DNA-PK). However, it is now recognized that the cellular radiation response is complex, and radiosensitivity may be also regulated at different levels in the radiation signal transduction pathway. In addition to DNA damage, exposure to IR triggers intracellular signaling cascades that overlap with pathways initiated by ligand engagement to a receptor. In this study, we provide evidence for the novel localization of the DNA-PK complex in lipid rafts. We also show this property is not a generalized characteristic of all DNA repair proteins. Furthermore, we have detected Ku86 in yeast lipid rafts. Our results suggest that the components of this complex might be recruited separately to the plasma membrane by tethering with raft-resident proteins. In addition, we found an irradiation-induced differential protein phosphorylation pattern dependent upon DNA-PKcs in lipid rafts. Thus, we speculate that another role for the DNA-PKcs subunit and perhaps for the holoenzyme is in the signal transduction of IR response.

Animals↗

PubMed1993

Locomotion and physical development in rats treated with ionizing radiation in utero.

Effects of ionizing radiation on the emergence of locomotor skill, and physical development were studied in laboratory rats (Fisher F-344 inbred strain). Rats were treated with 3 different doses of radiation (150 rad, 15 rad, and 6.8 rad) delivered on the 20th day of prenatal life. Results indicated that relatively moderate (15 rad) to high (150 rad) doses of radiation had effects on certain locomotion and physical development parameters. Exposure to 150 rad delayed pivoting, cliff-avoidance, upper jaw tooth eruption, and decreased body weights. Other parameters, such as negative geotaxis, eye opening, and lower jaw tooth eruption were marginally delayed in the 150 rad treated animals. Exposure to 15 rad delayed pivoting and cliff-avoidance.

Animals↗

PubMed1996

Power lines and ionizing radiation.

The magnetic field and ionizing radiation dose rate were measured near ground level in the vicinity of a utility power line. The dose rate was monitored using thermoluminescence detectors. Measurements were made at distances up to about 100 m from the main transmission line from the Kewaunee Nuclear Power Plant while the plant was in operation and while the plant was shut down for refueling. No evidence was found that the dose rate is significantly different in the presence of the magnetic field from the power line than in its absence.

Climate↗

PubMed1976

The new special names of SI units in the field of ionizing radiations.

New SI units for ionizing radiations have been recommended by the internation Commission on Radiation Units and Measurements (ICRU). These are the becquerel (symbol Bq), equal to the second to the power -1, and the gray (symbol Gy), equal to the joule per kilogram. It was recommended that the roentgen be replaced as the unit of exposure by the coulomb per kilogram (C/kg), for which no new name was proposed. The ICRU recommends that the units rad, roentgen, and curie be gradually abandoned over a period of ten years and that preparatory steps to this end be taken as soon as possible by various national and international bodies in order to facilitate a smooth, safe, and efficient transition.

Radiation Dosage↗

PubMed2005

Proteasome structures affected by ionizing radiation.

Exposure of cells to ionizing radiation slows the rate of degradation of substrates through the proteasome. Because the 26S proteasome degrades most short-lived cellular proteins, changes in its activity might significantly, and selectively, alter the life span of many signaling proteins and play a role in promoting the biological consequences of radiation exposure, such as cell cycle arrest, DNA repair, and apoptosis. Experiments were therefore undertaken to identify the radiation target that is associated with the proteasome. Regardless of whether they were irradiated before or after extraction and purification from human prostate cancer PC3 cells, 26S proteasomes remained intact but showed a rapid 30% to 50% dose-independent decrease in their three major enzymatic activities following exposure to 1 to 20 Gy. There was no effect on 20S proteasomes, suggesting that the radiation-sensitive target is located in the 19S cap of the 26S proteasome, rather than in the enzymatically active core. Because the base of the 19S cap contains an ATPase ring that mediates substrate unfolding, pore opening, and translocation of substrates into the catalytic chamber, we examined whether the ATPase activity of purified 26S proteasomes was affected. In fact, in vitro irradiation of proteasomes enhanced their ATPase activity. Furthermore, pretreatment with low concentrations of the free radical scavenger tempol was able to prevent both the radiation-induced decrease in proteolytic activity and the increase in ATP utilization, indicating that free radicals are mediators of these radiation-induced phenomena. Finally, we have shown that cell irradiation results in the accumulation of proteasome substrates: polyubiquitinated proteins and ornithine decarboxylase, indicating that the observed decrease in proteasome function is physiologically relevant.

Adenosine Triphosphatases↗

PubMed1996

Signal Transduction and Cellular Responses to Ionizing Radiation.

The current understanding of cellular responses to ionizing radiation fuses traditional radiobiological concepts with recent insight into underlying molecular mechanisms. Cell cycle arrest, induction of specific cascades of genes, and activation of DNA repair mechanisms have been reported after radiation exposure. Of particular importance is the mitogen-activated protein (MAP) kinase signaling pathway, in which the ras and raf oncogenes participate. Both of these genes have been implicated in the cellular resistance to killing by ionizing radiation. Furthermore, regulated NF-gammaB transcriptional activation may be important for the pleiotrophic responses of cells to ionizing radiation. Disruption of this signaling cascade may contribute to the radiation sensitivity syndrome seen in ataxia telangiectasia. In this review, these pathways are consolidated into ionizing radiation signal transduction pathways that lead from the cell membrane/cytosol to the nuclear DNA.

Journal Article↗

PubMed2001

Protective role of superoxide dismutases against ionizing radiation in yeast.

The protective role of superoxide dismutases (SODs) against ionizing radiation, which generates reactive oxygen species (ROS) harmful to cellular function, was investigated in the wild-type and in mutant yeast strains lacking cytosolic CuZnSOD (sod1Delta), mitochondrial MnSOD (sod2Delta), or both SODs (sod1Deltasod2Delta). Upon exposure to ionizing radiation, there was a distinct difference between these strains in regard to viability and the level of protein carbonyl content, which is the indicative marker of oxidative damage to protein, intracellular H2O2 level, as well as lipid peroxidation. When the oxidation of 2',7'-dichlorofluorescin was used to examine the hydroperoxide production in yeast cells, the SOD mutants showed a higher degree of increase in fluorescence upon exposure to ionizing radiation as compared to wild-type cells. These results indicated that mutants deleted for SOD genes were more sensitive to ionizing radiation than isogenic wild-type cells. Induction and inactivation of other antioxidant enzymes, such as catalase, glucose 6-phosphate dehydrogenase, and glutathione reductase, were observed after their exposure to ionizing radiation both in wild-type and in mutant cells. However, wild-type cells maintained significantly higher activities of antioxidant enzymes than did mutant cells. These results suggest that both CuZnSOD and MnSOD may play a central role in protecting cells against ionizing radiation through the removal of ROS, as well as in the protection of antioxidant enzymes.

Catalase↗

PubMed1993

Reactive oxygen intermediates target CC(A/T)6GG sequences to mediate activation of the early growth response 1 transcription factor gene by ionizing radiation.

The cellular response to ionizing radiation includes induction of the early growth response 1 gene (EGR1). The present work has examined the involvement of reactive oxygen intermediates (ROIs) in this response. Exposure of human HL-525 cells, an HL-60 subclone deficient in protein kinase C-mediated signaling, to both ionizing radiation and H2O2 was associated with increases in EGR-1 transcripts. These increases in EGR-1 expression were inhibited by the antioxidant N-acetyl-L-cysteine (NAC). Nuclear run-on assays demonstrate that NAC inhibits the activation of EGR1 transcription by these agents. Previous studies have shown that induction of EGR1 by x-rays is conferred by serum response or CC(A/T)6GG (CArG) elements. The present studies demonstrate similar findings with H2O2 and the finding that activation of the EGR1 promoter region containing CArG elements is abrogated by NAC. Moreover, we show that NAC inhibits the ability of a single CArG box to confer x-ray and H2O2 inducibility when linked to a heterologous promoter. Taken together, these findings indicate that ROIs induce EGR1 transcription by activation of CArG elements.

Actins↗

PubMed1995

Cell cycle checkpoints and repair of ionizing radiation damage.

Following exposure to ionizing radiation (IR), normal cells activate a delay in any phase of the cell cycle in conjunction with DNA repair mechanisms. Cell cycle delay or arrest is a programmed response that is mutable by a variety of genetic changes. DNA repair mechanisms that are responsible for the repair of otherwise lethal IR-induced double-strand breaks (DSBs) operate in a parallel pathway. The formulation of this pathway has recently been investigated, and new information regarding several mutant cell lines that are unable to execute IR-induced DSB repair are summarized. The scid mutation and defects in Ku proteins have been characterized. Molecular readouts of the properties of IR repair have been identified, including the hyperphosphorylation of the 34 kDa subunit of replication protein A. In addition, we have identified features of the G1/S IR-induced checkpoint that can be influenced by p53 status, genetic background or the levels of cell cycle proteins. A further understanding of the players in these pathways is expected to lead to the identification of molecular markers for ionizing radiation damage. Examination of the changes in these proteins may be valuable in a clinical setting for documenting radiation exposure.

Animals↗

PubMed2004

Expression of the oxidative base excision repair enzymes is not induced in TK6 human lymphoblastoid cells after low doses of ionizing radiation.

Most of the DNA damage produced by ionizing radiation is repaired by the base excision repair (BER) pathway. To determine whether the BER genes were up-regulated by low doses of ionizing radiation, we investigated their expression in TK6 human lymphoblastoid cells by measuring mRNA levels using real-time quantitative PCR. No induction at the transcriptional level of any of the base excision repair genes, NTH1 (NTHL1), OGG1, NEIL1, NEIL2, NEIL3, APE1, POLB, or accessory protein genes, LIG3, XRCC1 or XPG, was found at gamma-radiation doses ranging from 1 cGy to 2 Gy in a 24-h period. As has been measured in other cell lines, a dose-dependent induction of CDKN1A (WAF1) mRNA levels was observed in TK6 cells in the dose range of 0.5 to 2.0 Gy. We also examined BER enzyme activity on 8-oxoguanine-, dihydrouracil- and furan-containing oligonucleotide substrates and found no increase in extracts of TK6 cells after gamma-ray doses of 0.5-2.0 Gy. These data were corroborated by Western blot analysis of APE1 and NTH1, suggesting that the BER enzymes are also not up-regulated at the post-transcriptional level after ionizing radiation exposure.

Blotting, Western↗

PubMed2002

Immune modulation by ionizing radiation and its implications for cancer immunotherapy.

Ionizing radiation exhibits immunomodulatory properties, which could portend a future collaboration of cancer immunotherapy with radiation therapy. The danger model of immunity describes antigen-specific cellular immunity engendered by an inflammatory milieu. Dendritic cells (DCs) are attracted to this microenvironment, undergoing maturation after internalizing apoptotic and necrotic cellular debris. Mature DCs mediate antigen-specific cellular immunity via presentation of processed antigen to T cells. Administration of radiation has been utilized in vitro and in vivo to create an inflammatory setting, via induction of apoptosis, necrosis, cell surface molecules, and secretory molecules. Caspase-mediated cellular apoptosis is induced by radiation thro ugh multiple signaling pathways. Radiation upregulates expression of immunomodulatory surface molecules (MHC, costimulatory molecules, adhesion molecules, death receptors, heat shock proteins) and secretory molecules (cytokines, inflammatory mediators) in tumor, stromal, and vascular endothelial cells. Results of animal studies indicate possible radiation-mediated modulation of tumor antigen-specific immunity. Experimental data could indicate that the radiation-induced danger microenvironment engenders a DC-mediated antigen-specific immune response. Further enhancement of radiation-mediated inflammation and cell death can be achieved via administration of radiosensitizing pharmaceuticals. Radiation-mediated immune modulation currently remains unquantified and poorly understood. A major research effort will be required to elucidate mechanisms of action. With a thorough understanding of this phenomenon, we believe that ionizing radiation could be optimized for use with cancer vaccines and generate tumor antigen-specific cellular immunity.

Animals↗

PubMed2005

Mortality of workers exposed to ionizing radiation at the French National Electricity Company.

BACKGROUND: Exposure to ionizing radiation increases the risk of cancer in humans. Nuclear workers receive low doses over a relatively long period of time. METHODS: A mortality study of a cohort of workers exposed to ionizing radiation at Electricité de France (EDF) was conducted. The cohort consisted of 22,395 individuals monitored for radiation exposure between 1961 and 1994, and followed-up for an average of 11.7 years. RESULTS: Our study demonstrates a clear healthy worker effect (HWE) since mortality is less than half what is expected from National mortality statistics. The HWE is greater among workers who have spent most of their career in the nuclear sector. The analysis by cancer site shows no excess compared with the general population. No significant trend was observed according to level of exposure to ionizing radiation. CONCLUSIONS: The mortality of workers exposed to ionizing radiation at the French National Electricity company is very low compared to the French national mortality.

Adolescent↗