[Radiation doses of cosmonauts by ionizing radiation during professional activity (data base)].
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Astronauts↗
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Mammalian X ray sensitive mutants: a tool for the elucidation of the cellular response to ionizing radiation.
The complexity of the cellular response to ionizing radiation is indicated by many complementation groups identified among mammalian cells sensitive to ionizing radiation. Genetic complementation analysis of these mutants has been based on cell fusion and complementation of cell killing by X ray, whereas complementation of RDS after gamma rays has led to false results among AT cell lines and could not also be used in rodent cells. Studies on the relationship between cell killing and RDS following gamma irradiation have indicated that (a) RDS is not responsible for cell killing and (b) DNA replication in response to gamma rays is controlled by several genes. Complementation groups established in rodent cell mutants have led to the identification of the gene function in several mutants, and remarkable progress has been made in the understanding of DSB repair and its involvement in V(D)J recombination. The remaining complementation groups of X ray sensitive mutants await the determination of the role of the defective genes in the pathways operating in mammalian cells against ionizing radiation. One group of rodent mutants seems to be defective in the gene homologous to the ATM gene, and so far no more human counterparts have been found among rodent mutants. Newly characterized mutants, V-C8 and UV40, showed combined features of several human disorders, suggesting that their defective gene products could be involved in several pathways handling the response to DNA damage.
Animals↗
Increase of NKG2D ligands and sensitivity to NK cell-mediated cytotoxicity of tumor cells by heat shock and ionizing radiation.
In this study, we have investigated if current cancer therapeutic modalities including hyperthermia and ionizing radiation can increase the expression of NKG2D ligands in human cancer cell lines. The expressions of NKG2D ligands were induced by both heat shock and ionizing radiation in various cell lines including KM12, NCI-H23, HeLa and A375 cells with peaks at 2 h and 9 h after treatment, respectively, although inducibility of each NKG2D ligand was various depending on cell lines. During the induction of NKG2D ligands, heat shock protein 70 was induced by heat shock but not by ionizing radiation. These results were followed by increased susceptibilities to NK cell-mediated cytolysis after treatment with heat shock and ionizing radiation. These results suggest that heat shock and ionizing radiation induce NKG2D ligands and consequently might lead to increased NK cell-mediated cytotoxicity in various cancer cells.
Antigens, Surface↗
[Occupational exposure to ionizing radiation and the occurrence of cataract].
Radiation cataract is one of ensuing effects of ionizing radiation, since its threshold dose under which it does not occur, and above which it shows dose dependency, has been observed. Clinical course of radiation cataract is identical for all the types of ionizing radiation and is very typical. Minimal dose for progressive cataract formation is determined by the type of radiation, i.e., its relative biological efficacy, dose, and the duration of the exposure period. Theoretically, threshold dose existence does not exclude the incidence of cataract formation under significantly smaller doses, as well. The aim of this study was to analyze the incidence of cataract formation among the medical staff professionally exposed to ionizing radiation. Neither of the diagnosed cataracts had typical morphology, nor was the correlation established between the dose, exposure time, and the cataract formation. All the diagnosed cataracts were described as premature, and therefore ionizing radiation was considered as a co-factor in premature cataract formation in the examined groups.
Adult↗
Involvement of reactive oxygen intermediates in the induction of c-jun gene transcription by ionizing radiation.
Previous work has demonstrated that the cellular response to ionizing radiation includes transcriptional activation of the c-jun gene. The signaling events responsible for this response, however, remain unclear. The present studies have examined the effects of ionizing radiation on c-jun expression in a variant of HL-60 cells, designated HL-525, which is deficient in protein kinase C (PKC)-mediated signal transduction. The results demonstrate that these cells express low levels of PKC alpha and PKC beta transcripts and exhibit an attenuated induction of c-jun expression following treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA). In contrast, HL-525 cells respond to ionizing radiation with an increase in c-jun mRNA which is more pronounced than that in wild-type HL-60 cells. These cells similarly respond to ionizing radiation with increased expression of the jun-B, jun-D, c-fos, and fos-B genes. Nuclear run-on assays demonstrate that X-ray-induced c-jun expression in HL-525 cells is regulated by increases in the rate of c-jun gene transcription. Moreover, mRNA stability studies in irradiated HL-525 cells demonstrate that the half-life of c-jun transcripts is prolonged compared to that in wild-type cells. Studies with N-acetyl-L-cysteine (NAC), an antioxidant, suggest that X-ray-induced transcriptional activation of the c-jun gene is mediated at least in part through the formation of reactive oxygen intermediates (ROIs). In this context, H2O2 also induced c-jun expression in HL-525 cells, and this effect was inhibited by NAC.(ABSTRACT TRUNCATED AT 250 WORDS)
Cell Nucleus↗
Decreases in occupational exposure to ionizing radiation among Canadian dental workers.
OBJECTIVE: To describe doses of ionizing radiation and their possible associations with mortality rates and cancer incidence among Canadian dental workers. METHODS: The National Dose Registry (NDR) of Canada was used to assess occupational dose of ionizing radiation received by dental workers. The NDR cohort includes 42,175 people classified as dental workers. Subjects in the NDR were linked to both the Canadian Mortality Database and the Canadian Cancer Database to ascertain cause of death and cancer incidence, respectively. RESULTS: The cohort consisted of 9,051 male and 33,124 female dental workers. A total of 656 incident cases of cancer and 558 deaths were observed. The standardized mortality ratio associated with all-cause mortality was 0.53 (90% confidence interval [CI] 0.49-0.57). The incidence of cancer among dental workers was lower than that for the Canadian population for all cancers except melanoma of the skin (for melanoma, the standardized incidence ratio was 1.46 [90% CI 1.14-1.85]). Occupational doses of ionizing radiation among dentists and dental workers have decreased markedly since the 1950s. CONCLUSIONS: Dental workers receive very low doses of ionizing radiation, and these doses do not appear to be associated with any increase in cancer incidence; the increased incidence of melanoma is more likely related to other risk factors such as exposure to ultraviolet radiation from sunlight.
Adult↗
IONIZING RADIATION AS AN INDUSTRIAL HEALTH PROBLEM.
Ionizing radiation, first as x-rays, later in natural form, was discovered in Europe in the late 1890's. Immediate practical uses were found for these discoveries, particularly in medicine. Unfortunately, because of the crude early equipment and ignorance of the harmful effects of radiation, many people were injured, some fatally. Because of these experiences, committees and regulatory bodies were set up to study the problem. These have built up an impressive fund of knowledge useful in radiation protection.With the recent development of the peaceful uses of atomic energy, sources of radioactivity have appeared cheaply and in abundance. A rapidly growing number are finding industrial application. Because of their potential risk to humans, the industrial physician must acquire new knowledge and skills so that he may give proper guidance in this new realm of preventive medicine.The Radiation Protection Program of one such industry, the Hydro-Electric Power Commission of Ontario, is summarized.
Canada↗
Chromosomal changes in somatic cells in seminoma patients after treatment with ionizing radiation or cytostatics.
Seminomas are sensitive to both ionizing radiation and cytostatic drugs. The study's objective was to find out the effects of cytostatics or ionizing radiation by comparing the results of genome testing before treatment and immediately afterwards. Repeat cytogenetic testing six months after completion of treatment was used to find out changes resulting from reparatory processes after various types of treatment and the degree of elimination of defective lymphocytes from circulation. Three cytogenetic tests were used in our study to find out structural changes in chromosomes (percentage of aberrations), sister chromatid exchanges (SCE) and the number of micronuclei in binuclear lymphocytes (MN). In patients treated with ionizing radiation, strong inhibition of the mitotic activity of lymphocytes occurred after irradiation of para-aortal and ipsilateral inguinal lymph nodes. However, it is difficult to make a connection between the mitotic activity of lymphocytes and their total number, which was found to be within a normal range throughout the study. There is, therefore, another possibility, i.e. that this process actually involves impairment of intracellular enzymes and blockage of the synthesis of macromolecules in lymphocytes which have suffered a large degree of genome damage. Six months after a completed course of irradiation, mitotic activity was found to be mostly normal; however, there was still a very high percentage of aberrations compared with group II (patients treated with a cytostatic, paraplatin) or with respect to the control group, in which the average percentage of aberrations was 1.42 (excluding dicentrics and rings, which are found in all irradiated patients). From the cytological-mutagenetic point of view, chemotherapy proved to be less aggressive to patients. The results of recovery were visible earlier and the elimination of damaged cells was quicker.
Adolescent↗
Variability of the adaptive response to ionizing radiations in humans.
Human lymphocytes exposed to low doses of ionizing radiations from incorporated tritiated thymidine ([3H]dThd) or from X-rays become less susceptible to the induction of chromatid aberrations by high doses of X-rays. This indicates that low doses of ionizing radiation can produce an effect similar to the adaptive response observed with alkylating agents in prokaryotes, animal and plant cells. To determine whether there is individual variability in the adaptive response to ionizing radiations we exposed human lymphocytes from 18 different healthy donors to 'adapting' doses of [3H]dThd (0.01 microCi/ml) or X-rays (0.01 Gy) and subsequently to a 'challenge' treatment of 0.75 Gy of X-rays delivered 2 h before fixation. Four of the 18 donors did not show an adaptive response; in some cases in these individuals a synergistic response of increased, rather than decreased, damage was found. Two of these 4 donors showed no adaptive response in 3 subsequent experiments separated by 4-month intervals. This suggests that the human population exhibits a heterogeneity in the adaptive response to ionizing radiations which might be, at least in part, genetically determined.
Adult↗
Involvement of nuclear factor of activated T cells 3 (NFAT3) in cyclin D1 induction by B[a]PDE or B[a]PDE and ionizing radiation in mouse epidermal Cl 41 cells.
The results from animal studies have shown that mouse skin is highly susceptible to both ionizing radiation and benzo[a]pyrene-7,8-diol-9,10-epoxide (B[a]PDE). Previous studies have also indicated that cyclin D1 plays a crucial role in controlling cell proliferation and tumorigenesis. We, therefore, investigated here the effect of ionizing radiation and B[a]PDE on cyclin D1 transcription and potential involvement of NFAT3 in regulation of cyclin D1 transcription in mouse epidermal Cl 41 cells. We found that B[a]PDE exposure induced a high level of NFAT activation and cyclin D1 transcription in mouse epidermal Cl 41 cells. Ionizing radiation exhibited an enhancement for NFAT activation and cyclin D1 induction by B[a]PDE, even though ionizing radiation by itself had only a marginal effect. By stably knockdown of NFAT3 protein expression using specific NFAT3 small interfering RNA (siRNA), we found that cyclin D1 induction by B[a]PDE or B[a]PDE plus ionizing radiation was dramatically impaired. These results indicate that ionizing radiation is able to enhance cyclin D1 transcription induced by B[a]PDE, and NFAT3 is involved in the regulation of cyclin D1 transcription by B[a]PDE or B[a]PDE plus ionizing radiation.
7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
The place of ionizing radiation in the treatment of thyroid carcinoma.
The use of ionizing radiation is not confined to the treatment of metastatic disease. Indeed, in undifferentiated tumors the treatment of choice is ionizing radiation, utilizing refined dosimetry and the sophisticated equipment available today. However, one must not forget the important palliation and prophylaxis that ionizing radiation can achieve in patients with metastases from the differentiated as well as undifferentiated forms of thyroid carcinoma.
Carcinoma↗
Nonmelanoma skin cancer in relation to ionizing radiation exposure among U.S. radiologic technologists.
Ionizing radiation (IR) is an established cause of nonmelanoma skin cancer, but there is uncertainty about the risk associated with chronic occupational exposure to IR and how it is influenced by ultraviolet radiation (UVR) exposure. We studied 1,355 incident cases with basal cell carcinoma (BCC) and 270 with squamous cell carcinoma (SCC) of the skin in a cohort of 65,304 U.S. white radiologic technologists who responded to the baseline questionnaire survey in 1983-1989 and the follow-up survey in 1994-1998. Cox's proportional-hazards model was used to estimate relative risks of BCC and SCC associated with surrogate measures of occupational exposure to IR and residential UVR exposure during childhood and adulthood, adjusted for potential confounders including pigmentation characteristics. Relative risks of BCC, but not of SCC, were elevated among technologists who first worked during the 1950s (RR = 1.42; 95% CI = 1.12-1.80), 1940s (RR = 2.04; 95% CI = 1.44-2.88) and before 1940 (RR = 2.16; 95% CI = 1.14-4.09), when IR exposures were high, compared to those who first worked after 1960 (p for trend < 0.01). The effect of year first worked on BCC risk was not modified by UVR exposure, but was significantly stronger among individuals with lighter compared to darker eye and hair color (p = 0.013 and 0.027, respectively). This study provides some evidence that chronic occupational exposure to IR at low to moderate levels can increase the risk of BCC, and that this risk may be modified by pigmentation characteristics.
Adult↗
Copper ion-mediated sensitization of nuclear matrix attachment sites to ionizing radiation.
Exposure of mammalian cells to ionizing radiation induces nuclear matrix proteins and their attached transcribing DNA sequences to form cross-links. To characterize the cellular and matrix components necessary for DNA-protein crosslink (DPC) formation, DPC yields have been examined in isolated nuclear matrices and in the intermediate steps during cell fractionation. It was found that, in both unirradiated and irradiated cells, all components of DPC are retained in isolated nuclei, and the formed DPC are retained as well during the cell fractionation procedure resulting in nuclear matrices. In contrast, nuclear matrices isolated from unirradiated cells are deficient in the ability to form DPC upon irradiation, indicating that elements necessary for DPC production have been disrupted or removed during the isolation procedure. When isolated nuclei were irradiated, the yield of radiation-induced DPC was about 2-fold higher than that for intact cells, presumably due to the removal of soluble cellular scavengers during the isolation procedure. Treatment of nuclei with Cu2+ to stabilize nuclear structural organization during the preparation of the nuclear matrix caused additional DNA, especially the matrix-associated newly replicated DNA, to become bound to protein. Such treatment also enhanced radiation-induced DPC production which was sensitive to OH radical scavengers. Moreover, radiation-induced DPC production in Cu(2+)-treated nuclei was more sensitive to EDTA and catalase than in untreated nuclei. It is therefore proposed that excess DPC induction in Cu(2+)-treated nuclei occurs preferentially at the sites of Cu2+ binding to chromatin where hydroxyl radicals are produced repeatedly through the Fenton reaction.
Animals↗
[Cutaneous epitheliomas induced by ionizing radiation during radiotherapy. Presentation of 35 cases].
Thirty five cases of carcinomas of the skin, presumably induced by ionizing radiation therapy are reported. There was a precise topographic relationship between the site of irradiation and that of onset of tumor; in 31 cases, there were multiple neoplastic foci in the skin area exposed to ionizing radiation; a sufficiently long period of time had elapsed from the time of exposure to ionizing radiation to the clinical diagnosis of induced tumor; cases in which there were cutaneous carcinomas in other parts of the body as well as in the skin area exposed to the radiation were excluded from the series. Almost all patients had been subjected to ionizing radiation for treatment of benign diseases and 29 for arthrosis. The median age of the patients at the time of exposure to the ionizing radiation was 33,33 years. The radiation dose to which the patients had been subjected varied from 10 to 25 Gy; this dose is rather low, however it is in this dose range, according to Gray, a relatively high incidence of induced tumor is verified. The median interval between exposure to ionizing radiation and clinical finding of the tumor was 18.5 years. The carcinomas were observed almost always in the trunk and like spontaneous carcinomas at this site they were almost exclusively basal cell type.
Adult↗
Cytogenetic signature for ionizing radiation.
A stable, easily measurable biological 'signature' for past exposure to densely ionizing radiation would be of significant value to estimate environmental radiation risk. Defined here, the S-ratio is the ratio of complete to incomplete chromosome translocations. It constitutes a clastogenic signature that appears to be stable over time, independent of dose, and varies inversely with the relative biological effectiveness (RBE) of the radiation. In vitro measurements resulted in a ratio of approximately 2 for densely ionizing radiation (56Fe and 12C ions) in contrast to a value of approximately 10 for sparsely ionizing radiation (X- and gamma-rays). The measured ratio was approximately 2 for bleomycin and benzene. Such a distinctive clastogenic signature should facilitate better estimates of neutron dose for A-bomb survivors, as well as a causal connection between early exposure to densely ionizing radiation and late development of cancer.
Animals↗
Analyzing cell cycle checkpoints after ionizing radiation.
Several methods to measure cell cycle perturbation after exposure to ionizing radiation are presented in this chapter. These methods include the G1 checkpoint assay by 5' bromode-oxyuridine (BrdUrd) labeling followed by flow cytometric analysis, the S-phase checkpoint assay by measuring DNA synthesis in response to ionizing radiation, and the G2/M checkpoint assay by quantitating histone H3 phosphorylation after ionizing radiation.
Bromodeoxyuridine↗
Melanoma and ionizing radiation: is there a causal relationship?
This review was initiated in response to concerns that ionizing radiation could be a cause of melanoma. Studies presenting the relative risks for melanoma after external ionizing radiation exposure were in seven categories: (1) The Canadian Radiation Dose Registry, (2) nuclear industry workers, (3) subjects near nuclear test blasts, (4) survivors of the atomic bombings of Japan, (5) airline pilots and cabin attendants, (6) recipients of medical radiation, and (7) radiological technicians. Relative risks for leukemia in each of the studies were used to confirm the likelihood of exposure to ionizing radiation. When studies within a category were compatible, meta-analytic methods were used to obtain combined estimates of the relative risk, and a meta-regression analysis of melanoma relative risk compared to leukemia relative risk was used to examine consistency across exposure categories. Generally, exposure categories with elevated relative risks of leukemia had proportionately elevated relative risks of melanoma. This suggests that people exposed to ionizing radiation may be at increased risk of developing melanoma, although alternative explanations are possible. Future epidemiological studies of ionizing radiation effects should include melanoma as an outcome of interest.
Aircraft↗
Radio-induced structural membrane modifications: a potential bioindicator of ionizing radiation exposure?
PURPOSE: This study focused on radio-induced membrane alterations in order to assess some related parameters as potential biological indicators of ionizing radiation effects in cases of accidental overexposure. MATERIALS AND METHODS: Radio-induced membrane alterations were assessed after gamma-irradiation of human blood. Biophysical techniques based on fluorescent probe incorporation into isolated living lymphocytes and erythrocytes membranes were applied. RESULTS: Using the technique of fluorescence polarization, the lipophilic phase of the membrane was shown to be more fluid whereas the lipid-protein interface of the membrane was shown to be more rigid after gamma-irradiation. Fluorescent anisotropy modifications showed dose-time effect relationships after radiation exposure. Ionizing radiation induced a decrease in steady-state anisotropy values but did not affect the probe's lifetime as assessed by fluorescence lifetime distribution technique. These data suggest that the anisotropy variations are representative of the local properties of the fluorescent probe's micro-environment. However, the distribution width showed a decrease pointing towards radiation-induced changes of membrane domain organization, probably due not only to membrane water penetration related to lipoperoxidation, but also to compositional changes and redistribution of membrane components. In contrast, the lack of radiation effect observed using the lateral diffusion index technique may be related to the integrated overview of the radio-induced modifications of the membrane provided by this technique, which pointed out radio-induced damage to the membrane in micro-domains. CONCLUSION: These findings suggest the utility of structural membrane modification measurements as an early bio-indicator of ionizing radiation exposure.
Cell Membrane↗