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At least 55 records · Page 3Linked to original sources
PubMed1989

Standards and calibration facilities of the Australian Radiation Laboratory for ionizing radiation beams.

The Australian Radiation Laboratory (ARL) maintains national standards of exposure and working standards of absorbed dose. Some of the exposure standards maintained by ARL have been compared recently with those of the Bureau International des Poids et Mesures (BIPM) for 100 to 250 kV x-rays and 60Co gamma rays. The absorbed dose standard for 60Co gamma rays is compared regularly with other standards through the International Atomic Energy Agency (IAEA) and World Health Organization (WHO). All results show good agreement. A range of calibration qualities is offered at ARL, extending from 10 kV x-rays to 60Co gamma rays. A system of regional facilities has been developed for radiation protection calibrations; each facility is supplied with a set of 137Cs sources and an ionization chamber and electrometer for use with x-rays. The system is now almost complete throughout Australia.

Australia↗
PubMedDate not supplied

[Radiation and immunity. Interference of ionizing radiation with key immune processes].

Recent evidences of the interference of ionizing radiation into the intimate immune processes are presented in the review. gamma-irradiation induces some events in V-gene rearrangement in T cells. Low-dose irradiation can result in the thymocyte differentiation and activation. Immediately after irradiation stromal thymic cell activity are stimulated and in the later stages it is depressed. Irradiation induces an expression of some functionally important molecules on a surface of the cells of immune system and thus influences the processes of cell interaction, costimulation, adhesion and transvascular migration. It is shown that many events of the signal transduction pathways resulting in radiation-induced and activation-induced apoptosis of lymphocyte are general. This data evidence that the possibility of the choice between the death and activation exists for the cells which are undergone to action of ionizing radiation.

Animals↗
PubMed2006

Iodide sensitizes genetically modified non-small cell lung cancer cells to ionizing radiation.

While external ionizing radiation has been used for treating non-small cell lung cancer (NSCLC), improved efficacy of this modality would be an important advance. Ectopic expression of the sodium iodide symporter (NIS) and thyroperoxidase (TPO) genes in NSCLC cells facilitated concentration of iodide in NSCLC cells, which markedly induced apoptosis in vitro and in vivo. Pre-incubation of the NIS/TPO-modified NSCLC cells in iodide followed by ionizing radiation generates bystander tumoricidal effects and potently enhances tumor cell killing. This iodide-induced bystander effect is associated with enhanced gap junction intercellular communication (GJIC) activity and increased connexin-43 (Cx43) expression. Thus, iodide may serve as an enhancer to markedly improve the efficacy of radiation therapy in combined therapeutic modalities.

Apoptosis↗
PubMed2004

Mitogen-activated protein kinases: specificity of response to dose of ionizing radiation in liver.

Ionizing radiation is known to activate both the cytotoxic stress-activated kinases (SAPK/JNK, p38) and the cytoprotective mitogen-activated protein kinases (MAPKs, ERKs), which send divergent signals to the nucleus. However, all these kinases could not be activated simultaneously and at all the doses. An attempt has been made in this study to establish the dose and temporal response of these kinases with a view to establish the identity of the transcription factors that remain activated because only these will be translated into an effect. The study indicates that the stress-activated kinases (SAPK/JNK and p38) are activated by very low doses (0.1 Gy) of ionizing radiation. An induction of expression of MKK4, precursor to SAPK and p38, was found at lower doses (0.1-0.5 Gy). However, the cytoprotective ERK2 showed a progressive increase in expression with dose, except at 3 Gy where it shows a marginal decline. The stress-activated kinases show an increased expression or activation at early periods, unlike ERK2, which shows a prolonged response to stimuli. This study reveals that in the in vivo condition there is a chronological order of activation of the kinases and a dose-dependent activation. The activations of the cytoplasmic kinases and the transcription factors, Elk-1 and c-Jun, both show prolonged activation and maximum response at high doses.

Animals↗
PubMed2005

Dose-dependent generation of RET/PTC in human thyroid cells after in vitro exposure to gamma-radiation: a model of carcinogenic chromosomal rearrangement induced by ionizing radiation.

Ionizing radiation is a well-known risk factor for thyroid cancer in human populations. Chromosomal rearrangements involving the RET gene, known as RET/PTC, are prevalent in thyroid papillary carcinomas from patients with radiation history. We studied the generation of RET/PTC in HTori-3 immortalized human thyroid cells exposed to a range of doses of gamma-radiation and harvested 2, 5-6, and 9 d later. RET/PTC1 and RET/PTC3 were detected by RT-PCR followed by Southern blotting and hybridization with internal oligonucleotide probes. No RET/PTC was found in cells harvested 2 and 5-6 d after irradiation, whereas 59 RET/PTC events were detected in cells collected 9 d after exposure. The average rate of RET/PTC induction was 0.1 x 10(-6) after exposure to 0.1 Gy, 1.6 x 10(-6) after 1 Gy, 3.0 x 10(-6) after 5 Gy, and 0.9 x 10(-6) after 10 Gy. When adjusted for cell survival, the rate after 10 Gy was comparable with those after 5 Gy. RET/PTC1 was more common than RET/PTC3 after each dose, comprising 80% of all rearrangements. In this study, we demonstrate a dose-dependent induction of RET/PTC rearrangements in human thyroid cells after exposure to 0.1-10 Gy gamma-radiation. This provides additional evidence for a direct link between this genetic event and radiation exposure and offers a powerful experimental system for studying radiation-induced carcinogenesis in the thyroid gland.

Cell Proliferation↗
PubMed1962

Effect of ionizing radiation on immunity.

Ionizing radiation has a deleterious effect on the immunity mechanism, particularly when large but sublethal doses are applied over a short period of time. The hematopoietic system is extremely sensitive, and a fall in the lymphocytes is one of the most characteristic manifestations. The normal balance of the microflora of the intestinal and respiratory tracts is disturbed, which results in a bacteremia and may lead to death of the host. Active immunity is seriously interfered with if the irradiation occurs shortly before the injection of an antigen. There is also reduced resistance to pathogenic micro-organisms, which may lead to fatal infections. Prolonged irradiation at low levels does not seem to affect immunity adversely. Active immunization should be carried out well in advance of exposure to radiation, and supportive treatment commenced immediately after exposure to large doses.

Humans↗
PubMed1999

Ultraviolet and ionizing radiation enhance the growth of BCCs and trichoblastomas in patched heterozygous knockout mice.

Basal cell carcinomas, the commonest human skin cancers, consistently have abnormalities of the hedgehog signaling pathway and often have PTCH gene mutations. We report here that Ptch+/- mice develop primordial follicular neoplasms resembling human trichoblastomas, and that exposure to ultraviolet radiation or ionizing radiation results in an increase in the number and size of these tumors and a shift in their histologic features so that they more closely resemble human basal cell carcinoma. The mouse basal cell carcinomas and trichoblastoma-like tumors resemble human basal cell carcinomas in their loss of normal hemidesmosomal components, presence of p53 mutations, frequent loss of the normal remaining Ptch allele, and activation of hedgehog target gene transcription. The Ptch mutant mice provide the first mouse model, to our knowledge, of ultraviolet and ionizing radiation-induced basal cell carcinoma-like tumors, and also demonstrate that Ptch inactivation and hedgehog target gene activation are essential for basal cell carcinoma tumorigenesis.

Animals↗
PubMedDate not supplied

[Triiodothyronine reception after exposure to low doses of ionizing radiation].

Effects of ionizing radiation in doses 0.5 and 1 Gy on triiodothyronin reception by rat peripheral blood lymphocytes were examined 3, 10, and 30 days after exposure. Binding capacity of 125-I labeled triiodothyronin by lymphocyte receptors was found to change depending on the dose of external irradiation and time elapsed since the exposure. The most marked and earliest changes in the parameters of hormonal-receptor interaction were observed after irradiation in dose 1 Gy.

Animals↗
PubMed2005

[Risk from prenatal exposure to ionizing radiation].

Exposure to ionizing radiation during pregnancy always is a worrisome event. Knowledge of teratogenic and carcinogenic mechanisms based on reliable scientific data (ICRP 84) allows appropriate management of patients following exposure to ionizing radiation. Radiation exposure in the setting of diagnostic imaging studies is not associated with an increased risk of fetal malformation; however, the risk of childhood malignancy is minimally increased. This information must be provided to parents so they may reach an informed decision with regards to the outcome of the pregnancy. The analysis of the quality and quantity of exposure should be limited to imaging examinations where the abdomen was exposed. Management will be based on the type of exposure. Guidelines are provided for various exposure situations and all radiologists must be able to manage such situations.

Female↗
PubMed1998

Butyrate attenuates BCLX(L) expression in human fibroblasts and acts in synergy with ionizing radiation to induce apoptosis.

Ionizing radiation is a poor inducer of apoptosis in many cell types. In this study we investigated what effect the differentiation agent butyrate had on the cellular levels of the apoptosis regulators BCL2, BCLX(L) and BAX and on radiation-induced apoptosis. It was found that butyrate significantly lowered the level of the apoptosis antagonist BCLX(L) in a time- and dose-dependent manner in diploid human fibroblasts. The reduction of the level of BCLX(L) protein by butyrate correlated with an increased induction of apoptosis in cells irradiated with ionizing radiation. Butyrate also acted in synergy with ultraviolet (UV) light and cisplatin to induce apoptosis in human fibroblasts. Radiosensitization was obtained when butyrate was added before and/or after irradiation, although the combination of treatment both before and after irradiation was the most effective. Our results suggest that butyrate acts in synergy with ionizing radiation, UV light and cisplatin to induce apoptosis, perhaps by lowering the level of the apoptosis antagonist BCLX(L) in cells.

Apoptosis↗
PubMed2003

Death receptor ligands: new strategies for combined treatment with ionizing radiation.

The major goal of modern radiation oncology is the achievement of a maximal tumor control with minimal normal tissue damage. However, normal tissue tolerance may preclude the application of tumoricidal radiation doses. In order to overcome this limitation, strategies either to increase normal tissue tolerance or to reduce the radiation dose required may prove beneficial. In this regard, attempts to minimize the required radiation dose by reducing the number of malignant clonogenic cells are promising. Therefore, therapies which induce programmed cell death (apoptosis) in tumor cells, may prove to be suitable approaches. TRAIL (TNFalpha-related apoptosis inducing ligand)/Apo2L is a very promising member of the family of death ligands. The ligand preferentially induces apoptotic cell death in a wide range of tumor cells but not in normal cells. TRAIL/Apo2L triggers apoptosis even in cells not undergoing apoptosis in response to radiation, since ionizing radiation induce apoptosis by a different pathway as death ligands although an overlapping set of molecules is involved. Combination of both modalities has been shown to induce additive or synergistic apoptotic effects and eradication of clonogenic tumor cells thereby increasing the therapeutic efficacy. The present article reviews this novel biological strategy for optimized radiotherapy based on the combination of ionizing irradiation and death receptor triggered cell death.

Animals↗
PubMed1992

Down-regulation of cell cycle control genes by ionizing radiation.

The cellular responses to ionizing radiation include growth arrest, DNA repair, and lethality. However, little is known about the signaling events responsible for these responses. The present studies have examined the effects of ionizing radiation on the expression of genes involved in cell cycle control. The results demonstrate that the treatment of asynchronous cells with 20 Gy ionizing radiation is associated with transient down-regulation of the cdc2, cyclin A, cyclin B, and cdc25 genes. This effect was associated with transient induction of the c-jun gene. RNA stability studies demonstrate that the down-regulation of gene expression following ionizing radiation exposure is at least in part due to a decrease in transcript half-life. Other studies were performed with elutriated cells enriched for populations in G1 and S phases. Treatment of G1 enriched cell populations with 10 Gy resulted in a selective decrease in cyclin B mRNA levels, whereas this effect on cyclin B expression was less pronounced at 5 Gy and undetectable at 1 Gy. Similar results were obtained with S phase enriched cells. Taken together with clonogenic survival studies, these findings indicate that down-regulation of cell cycle control gene expression is associated with lethality, whereas lower doses of ionizing radiation have little, if any, effect on the expression of these genes. The findings also suggest that DNA damage may activate signaling events which regulate expression of cell cycle control genes.

CDC2 Protein Kinase↗
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↗