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Results for “Radiation, Ionizing”

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PubMed2004

Demographic analysis and modeling of human populations exposed to ionizing radiation.

The health effects of ionizing radiation on human populations are often analyzed using epidemiological statistical methods. Because of the complexity of the health consequences of ionizing radiation and the prolonged period during which the consequences emerge, we propose to evaluate these health effects using mathematical models that are based on the best theoretical reasoning and prior biological evidence about disease mechanisms. We believe this will improve the ability of the model to identify health effects and reduce erroneous inferences.

Demography↗

PubMed1999

[Cell cycle regulation after exposure to ionizing radiation].

When cells are exposed to ionizing radiation, they initiate a complex response that includes the arrest of cell cycle progression in G1 and G2, apoptosis and DNA repair. DNA is an important subcellular target of ionizing radiation, but oxydative damage to plasma membrane lipids initiates signal transduction pathways that activate apoptosis and that may play a role in cell cycle regulation. How is DNA damage converted into intracellular signals for cell cycle arrest? The ataxia telangectasia mutant (ATM) protein and/or the DNA-dependent protein kinase (DNA-PK), that are both activated by DNA damage, may initiate cell cycle arrest by activating the p53 tumor suppressor protein. The p53 protein acts as a transcription factor and regulates expression of several components implicated in pathways that regulate cell cycle progression. The best known, p21WAF1/CIP1 protein, is an inhibitor of cyclin-dependent kinases (CDK), a family of protein kinases known as key regulators of cell cycle progression. p21WAF1/CIP1 was shown to be able to inhibit several CDK, but is most effective toward G1/S cyclins. Other CDK inhibitors, p27KIP1 and p15INK4b are activated by irradiation and contribute to the G1 arrest. Moreover, radiation-induced G2 arrest was shown to require inhibitory phosphorylation of the kinase cdc2 via an ATM-dependent pathway. Mutations in cell cycle regulatory genes are common in human cancer and cell cycle regulatory deficiency can lead to increase resistance to ionizing radiation in cancer cells. The major function of p53-dependent G1 arrest may be elimination of cells containing DNA damage whereas G2 arrest following radiation has been shown to be important in protecting cells from death. Cell cycle checkpoints offer a new set of potential targets for chemotherapeutic compounds, especially the G2 checkpoint. Thus, abrogation of the G2 checkpoint with methylxanthines such as caffeine or protein kinase inhibitors such as staurosporine and UCN-01 (7-hydroxystaurosporine) was found to sensitize cells to ionizing radiation. These data did not lead to clinical applications, but confirm targeting of the G2 checkpoint may be an important strategy for cancer therapy.

Apoptosis↗

PubMed1992

Fixation for biological ultrastructure. II. Cross-linking of bovine serum albumin by nanosecond pulses of ionizing radiation.

Very large doses of ionizing radiation were delivered quickly to concentrated albumin solutions by pulses of 500 keV in air. The electrons penetrated the aluminium foil bottom of the test cell and into the solution. A dose of 4.6 Mrad (4.6 x 10(4) Gy) produced a gel in the albumin solution comparable to the long-term effect of 0.36% glutaraldehyde in the same albumin solution. The cross-links created by the radiation leading to gel formation are probably irreversible and quite different from those leading to gelation in the glutaraldehyde-albumin reaction. Single large pulses of ionizing radiation may be useful for fast fixation of cells and tissues for microscopy.

Equipment Design↗

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↗

PubMed1991

[Medical examination of the workers occupationally exposed to ionizing radiation].

The hazardous effects of ionizing radiation to man are well recognized, and they are divided into two groups, the stochastic effects (hereditary and carcinogenic effect) and non-stochastic effects (somatic effects such as depression of hematopoiesis, chronic dermatitis and cataracta). The basic framework of the International Commission on Radiological Protection (ICRP) is intended to prevent the occurrence of non-stochastic effects, by keeping doses below the relevant thresholds, and to ensure that all reasonable aspects are taken to reduce the incidence of stochastic effects. In Japan, the regulatory provisions of radiological protection of the workers occupationally exposed to ionizing radiation are based on the recommendation of ICRP adopted in 1977. According to these regulations, the dose equivalent limits of occupational exposure of man has been decided at 50 mSv/year. The monitoring of exposure to the individual and the procedure of medical examination of the workers are briefly described and discussed.

Environmental Monitoring↗

PubMed1999

Nurture with ionizing radiation: a provocative hypothesis.

Whole body exposure to low-dose ionizing radiation appears to decrease overall cancer incidence. The data come from at least eight large studies of populations exposed to various forms of radioactive material and from more limited studies of occupational and environmental exposures to plutonium, radium, and radon. Earlier experiments in animals strongly support the protective effect that is apparent in humans. Also, experimental reports from invertebrates kept in radiation-deficient conditions suggest that ionizing radiation is essential for optimal growth and development. The combined evidence points to the presence of no-adverse-effect thresholds and of hormesis or beneficial effects at doses below those thresholds. Furthermore, according to the geological record, the high background radiation under which life first evolved has progressively attenuated up to the present. Thus it is intriguing to postulate that modern humans may live under conditions of partial deficiency of ionizing radiation; low doses of ionizing radiation may likely function as inducers of repair and detoxification mechanisms, much as low-level antigenic challenges are responsible for enhanced immune competence. This hypothesis runs contrary to the prevailing consensus of regulatory default assumptions, which negate the possibility of no-effect thresholds for agents that are carcinogenic at certain levels of exposure. Still, those are dogmatic policy assumptions without scientific or even empirical justification, whereas the hypothesis advanced here has consistent observational and experimental support. The implication is that a partial deficiency of ionizing radiation could be remedied by a safe supplementation, possibly through dietary means. Dose-response data from studies of nuclear workers and populations subjected to unusual exposures suggest that safe supplementation with about 0.4 cGy/mo would be beneficial and conservative.

Animals↗

PubMed2006

Novel approach to analyzing the carcinogenic effect of ionizing radiations.

PURPOSE: Cancer incidence of ionizing radiations exposure is considered to be proportional to the absorbed dose. However, there are disagreements between substantial amounts of epidemiological studies. In this study, we question the basic relationship of the risk estimate with total accumulated dose, and reanalyse available data on the basis of a daily dose concept. MATERIALS AND METHODS: The data analysed were relative mortality risk from all cancers vs. total-body dose on a daily basis. References have been selected on the basis of objective criteria. RESULTS: We found that this relationship removes major discrepancies. It revises estimates of low-level exposures, with consequences regarding nuclear power plants safety, wastes management, medical applications or homeland security. CONCLUSIONS: The idea that the dose rate may have a significant impact on health effects of ionizing radiations is not new, but has always been considered as a parameter in models based on integrated dose. The novel approach in this paper is to consider the primary relevant parameter as an average of dose rate over a time period of one day. This is an argument to revise the whole philosophy in radioprotection, and place regulatory limits on specific locations instead of annual limits relevant to individual persons.

Humans↗

PubMed2003

NF-kappaB activation plays an antiapoptotic role in human leukemic K562 cells exposed to ionizing radiation.

Exposure of cells to ionizing radiation (IR) determines cellular lesions, such as DNA and membrane damage, which involve a coordinate network of signal transduction pathways responsible for resistance to or delay of apoptosis, depending on cell type and administered dose. Since, after IR exposure, the apoptotic profile appeared different in the two chosen cell lines K562 and Jurkat along with caspase-3 activation, we paid attention to the influence exerted by Protein kinase C delta on transcription factor NF-kappaB activation. Interestingly, K562 resist to IR carrying out a survival strategy which includes PKC delta/NF-kappaB pathway activation, probably mediated by novel IKKs and a role for PI-3-kinase in activating PKC delta at Thr 505 by PDK-1 phosphorylation is suggested. In addition, since caspase-3 is not activated in these cells upon ionizing radiation exposure, it could be supposed that NF-kappaB antagonizes apoptosis induction interfering with pathways which lead to caspase activation, may be by inducing expression of IAP, caspases 3, 7, 9, inhibitor. Thus NF-kappaB activation explains the resistance displayed by K562 to IR and drug potential interference directed to this protein could overcome apoptosis resistance in clinical settings.

Apoptosis↗

PubMed1982

Physiological benefits from low levels of ionizing radiation.

Extensive literature indicates that minute doses of ionizing radiation benefit animal growth and development, fecundity, health and longevity. Specific improvements appear in neurologic function, growth rate and survival of young, wound healing, immune competence, and resistance to infection, radiation morbidity, and tumor induction and growth. Decreased mortality from these debilitating factors results in increased average life span following exposure to minute doses of ionizing radiation. The above phenomena suggest the possibility that ionizing radiation may be essential for life. Limited data with protozoa suggest that reproduction rates decrease when they are maintained in subambient radiation environments. This may be interpreted to be a radiation deficiency. Evidence must now be obtained to determine whether or not ionizing radiation is essential for growth, development, nutrient utilization, fecundity, health and longevity of higher animals. Whether or not ionizing radiation is found to be essential for these physiologic functions, the evidence reviewed indicates that the optimal amount of this ubiquitous agent is imperceptibly above ambient levels.

Animals↗

PubMed1994

Ionizing radiation induces apoptotic cell death in human TcR-gamma/delta+ T and natural killer cells without detectable p53 protein.

The p53 tumor suppressor gene has been shown to be involved in programmed cell death, apoptosis, in murine immature thymocytes after treatment with ionizing radiation. Ionizing radiation also induces apoptosis in peripheral mature lymphocytes. In this work, we investigated the p53 participation in radiation-induced apoptosis in human peripheral blood lymphocytes (PBL) subpopulations. Exposure to gamma-irradiation resulted in an appreciable induction of apoptotic cell death in TcR-alpha/beta+ (CD4+ and CD8+) T cells, TcR-gamma/delta+ T cells, B cells and natural killer (NK) cells, as assessed by DNA fragmentation as well as the morphological characteristics. Importantly, it was found that there was a marked difference among PBL subpopulations as regards the induction of p53 protein by gamma-irradiation. Similar to previous observations for murine thymocytes, p53 induction in TcR-alpha/beta+ T cells and B cells after gamma-irradiation was evident by Western blot analysis. Radiation-induced apoptosis in TcR-alpha/beta+ T cells and B cells was efficiently inhibited by cycloheximide, indicating the requirement of de novo protein synthesis, including p53 protein, for radiation-induced apoptosis in both subpopulations. In marked contrast, no identifiable levels of p53 protein were induced in either TcR-gamma/delta+ T or NK cells after gamma-irradiation. In addition, it was demonstrated that radiation-induced cell death in TcR-gamma/delta+ T and NK cells could be prevented by interleukin-2, but not by cycloheximide. These results imply that radiation-induced lymphocytic apoptosis can be mediated by p53-dependent or -independent mechanisms.

Adult↗

PubMed1982

Ionizing radiation and its risks.

Penetrating ionizing radiation fairly uniformly puts all exposed molecules and cells at approximately equal risk for deleterious consequences. Thus, the original deposition of radiation energy (that is, the dose) is unaltered by metabolic characteristics of cells and tissue, unlike the situation for chemical agents. Intensely ionizing radiations, such as neutrons and alpha particles, are up to ten times more damaging than sparsely ionizing sources such as x-rays or gamma rays for equivalent doses. Furthermore, repair in cells and tissues can ameliorate the consequences of radiation doses delivered at lower rates by up to a factor of ten compared with comparable doses acutely delivered, especially for somatic (carcinogenic) and genetic effects from x- and gamma-irradiation exposure. Studies on irradiated laboratory animals or on people following occupational, medical or accidental exposures point to an average lifetime fatal cancer risk of about 1 x 10(-4) per rem of dose (100 per 10(6) person-rem). Leukemia and lung, breast and thyroid cancer seem more likely than other types of cancer to be produced by radiation. Radiation exposures from natural sources (cosmic rays and terrestrial radioactivity) of about 0.1 rem per year yield a lifetime cancer risk about 0.1 percent of the normally occurring 20 percent risk of cancer death. An increase of about 1 percent per rem in fatal cancer risk, or 200 rem to double the "background" risk rate, is compared with an estimate of about 100 rem to double the genetic risk. Newer data suggest that the risks for low-level radiation are lower than risks estimated from data from high exposures and that the present 5 rem per year limit for workers is adequate.

Embryo, Mammalian↗

PubMed2006

[Transgenerational effects of parental exposure to ionizing radiation].

The deleterious effects of exposure to ionizing radiation on human health have been known for many years. The main long term effect of this exposure is an increase in the risk for developing benign and malignant tumors in the exposed population. This review summarizes the existing data on the possible effects of ionizing radiation on the second generation, focusing on cancer risk. The two mechanisms through which parents' exposure to radiation could affect their children's health are intrauterine exposure of the fetus and preconception exposure of the gonads. Intrauterine exposure to ionizing radiation has teratogenic and carcinogenic effects. Most case-control studies have shown a 40-50% increase in the risk of cancer following intrauterine exposure to medical diagnostic radiation at doses of 10-20mGy. Results of these studies have greatly contributed to the strict radiation protection guidelines at pregnancy existing today. Although animal studies have shown that gonadal exposure to high doses can cause heritable genetic changes, this effect has not been demonstrated unequivocally in epidemiological studies. A case-control study suggested an association between preconception irradiation and leukemia/non-Hodgkin's lymphoma in children of male workers at a nuclear plant in the UK (the Gardner hypothesis). This report generated substantial interest and research; however, subsequent occupational studies failed to confirm the association. Negative results were also reported in studies of the atomic bomb survivors and survivors of childhood cancer. In summary, epidemiological studies do not support the association between gonadal exposure to ionizing radiation and the development of cancer and other genetic diseases among offspring.

Adult↗

PubMedDate not supplied

Combined effects of ultrasound and ionizing radiation on lymphocyte chromosomes.

The effects of ionizing radiation and ultrasound upon the induction of chromosomal-type aberrations and sister chromatid exchanges were investigated. No statistically significant increase in the frequencies of dicentric and ring chromosomes or sister chromatid exchanges was discovered after ultrasound exposure alone at the diagnostic level. Nor could elevated frequencies of these phenomena be found following exposure to ultrasound before or after ionizing radiation, compared with those resulting from an equivalent dose of ionizing radiation alone. However, simultaneous exposure to ultrasound and ionizing radiation seemed to induce a slight enhancement of sister chromatid exchanges, although no significant change was noted in the yields of dicentric and ring chromosomes.

Abnormalities, Radiation-Induced↗

PubMed1997

A cell line selected for resistance to ionizing radiation exhibits cross resistance to other genotoxic agents and a mutator phenotype for loss of heterozygosity events.

An ionizing radiation resistant derivative was obtained from the mouse P19H22 (aprt hemizygote) embryonal carcinoma cell line by repeated exposure to 137Cs gamma radiation. Ionizing radiation resistance in the 6Gy-R cell line was not correlated with a failure to undergo cell cycle arrest or a loss of the p53 response after exposure to 137Cs gamma radiation. Moreover, the cells did not display increased resistance to bleomycin, a double strand break inducing agent. However, the cells did display increased resistance to ultraviolet radiation, ethyl methanesulfonate, and 95% oxygen. A mutational analysis demonstrated a > 700 fold-fold increase in the frequency of aprt mutants for the 6Gy-R cells, but no change in the frequency of hprt or dhfr mutants. A molecular analysis suggested that the aprt mutations in the 6Gy-R cells arose by recombinational events. A possible association between radiation resistance, DNA repair, and a mutator phenotype for large-scale mutational events is discussed.

Adenine Phosphoribosyltransferase↗

PubMed2006

Effects of ionizing radiation on cellular structures, induced instability and carcinogenesis.

Ionizing radiation is perhaps the most extensively studied human carcinogen. There have been a number of epidemiological studies on human populations exposed to radiation for medical or occupational reasons, as a result of protracted environmental exposures due to radiation accidents, or after atomic bombings. As a result of these studies exposure to ionizing radiation has been unambiguously linked to cancer causation. While cancer induction is the primary concern and the most important somatic effect of exposure to ionizing radiation, potential health risks do not only involve neoplastic diseases but also somatic mutations that might contribute to birth defects and ocular maladies, and heritable mutations that might impact on disease risks in future generations. Consequantly it is important we understand the long-term health risks associated with exposure to ionizing radiation.

Cell Transformation, Neoplastic↗

PubMed1994

[Non-ionizing radiation protection in medicine].

Non-ionizing radiation is extensively used in medicine for diagnostic and therapeutic purposes. Health risks from exposure to different sources of non-ionizing radiation are still not well known. High exposure to non-ionizing radiation produces acute effects on sensitive organs, mostly depending on radiation intensity, frequency and exposure duration. Prolonged low-level occupational exposure may also be hazardous. It is therefore necessary for the medical personnel to be aware of their occupational risk and to know how to apply protective measures in order to protect own health as well as that of the patients.

Health Personnel↗

PubMed1996

Activation of Raf by ionizing radiation.

The critical pathways through which ionizing radiation induces malignant transformation and cell death are not well defined. Raf-1, a cytoplasmic serine-threonine protein kinase, mediates the transmission of mitogenic signals initiated at the cell membrane to the nucleus, resulting in the activation of transcription factors that regulate cell growth and proliferation. Moreover, Raf-1 overexpression and activation increases the survival response of mammalian cells to the toxic effects of ionizing radiation by an as-yet unknown mechanism (refs 3, 4 and V. Soldatenkov et al.; manuscript submitted). Somewhat analogous to mitogen-induced signalling, radiation stimulates protein-tyrosine kinase(s) and transcription factors. No direct biochemical link has been established, however, between radiation-stimulated protein tyrosine phosphorylation and downstream signals. Here we report a series of radiation-responsive events in which protein-tyrosine phosphorylation is followed by membrane recruitment, then tyrosine phosphorylation and activation of Raf-1 in vivo. Our results show that radiation-stimulated protein-tyrosine kinase(s) modify Raf-1, and implicate Raf-1 in the ionizing-radiation signal-transduction pathway.

Biological Transport↗

PubMedDate not supplied

Peripheral blood lymphocyte subsets in radiologists exposed to ionizing radiation.

To investigate whether low dose ionizing radiation caused perturbation of peripheral blood lymphocytes in radiology unit staff, the T-helper/suppressor ratio was examined in eight radiologists exposed to low dose radiation over a period of 6 to 27 years (mean 12 years). No significant difference was noted in the T-cell subsets between exposed radiologists and non-exposed control subjects. The effect of low dose ionizing radiation on peripheral blood lymphocyte subsets seems to be virtually negligible. Further, measurement of the T-helper/suppressor ratio is not a reliable way of demonstrating any damage to bone marrow caused by low dose ionizing radiation.

Adult↗