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PubMed2005

Full-color painting reveals an excess of radiation-induced dicentrics involving homologous chromosomes.

PURPOSE: To determine the ratio of homologous to heterologous dicentric chromosomes induced in human cells by ionizing radiation. This ratio is influenced by, and thus potentially informative about, underlying DNA damage/repair/misrepair processes and also the geometry of individual chromosome domains within the interphase nucleus. MATERIALS AND METHODS: 24-color mFISH (multiplex fluorescent in situ hybridization) was used to determine the ratio of 1-color (homologous) to 2-color (heterologous) dicentrics produced in human lymphocytes or fibroblasts by gamma-rays, alpha particles, or iron ions at various doses. Assuming that randomness independent of homology holds, the expected homologue:heterologue ratio for diploid human male cells is approximately 0.024, as shown by deriving a formula applicable to simple interchanges and then extending the result, via Monte Carlo simulation, to the general situation where complex aberrations are also considered. RESULTS AND CONCLUSIONS: There was a substantial excess of homologous dicentrics, with probability of occurrence by chance less than 0.02 for each of the three radiations and only about 10(-8) for all the data combined. Overall, approximately 18 homologous dicentrics were expected but 47 were found, including 11 involving chromosome 1. Observed excesses were similar for both sparsely and densely ionizing radiations. Geometric proximity of homologues is a possible explanation for the overabundance; in that case more extensive statistics should eventually uncover a linear energy transfer (LET) dependence. An alternative possibility, not ruled out by the present data, is homology-dependent misrepair.

Cell Culture Techniques↗

PubMed1982

Dominant lethal and ovarian effects of plutonium-239 in female mice.

In two separate experiments (C3H x 101)F1 female mice were injected intravenously with 239Pu in trisodium citrate, then mated in pairs to strain CBA males, to test for dominant lethality. In the first experiment 10 muCi kg-1 and in the second 20 muCi kg-1 body mass was injected. Matings were after 6 days in the first experiment (estimated ovarian absorbed dose of 0.1 Gy) and after 3, 6 or 12 weeks in the second (estimated ovarian doses of 1.11, 2.45 and 5.91 Gy respectively). No evidence of dominant lethal induction was found in the first experiment, but in the second there was a significant increase over controls in pre-implantation loss in all three series. Post-implantation lethality increased significantly (by 12 per cent) only after 12 weeks' exposure. With the 6- and 12-week exposures (especially the latter) luteal counts fell and fewer females became pregnant than in controls. This is attributed to oocyte killing by the alpha-particles. Histological and autoradiographic investigations showed a marked reduction in ovarian size and follicular numbers with fission-tracks clustered mainly over the medullary stroma. The pre-implantation loss may stem from lowered fertilization of oocytes because of their damage, so that the best measure of dominant lethality is that based on post-implantation death. Thus there is only slight evidence for the induction of genetic damage, which is in line with previous findings after chronic exposures of female mice.

Animals↗

PubMed1986

Some considerations of radiation-induced cell transformation in vitro.

Experimental data concerning the influence of the cell density on the induction rate of cell transformations in C3H mouse embryo cell lines (1OT1/2) after X-irradiation have been reanalysed. The mathematical analysis showed that the transformation frequency can be expressed as the product of two functions, one of which is dependent on radiation dose alone, and the other of which is dependent on the number of cell division cycles alone, in that the probability of the expression of malignant transformation is constant per cellular mitosis. Therefore the transformation frequency measured for different experimental conditions can be normalized and consequently compared; one example of data reduction after irradiation by alpha-particles is demonstrated.

Animals↗

PubMed1989

The initial physical damage produced by ionizing radiations.

Biophysical studies of different ionizing radiations and their differences in biological effect can provide useful information and constraints on the nature of the initial biologically relevant damage and hence the subsequent biochemistry and repair processes. It is clear that the nature of the predominant critical component produced by densely ionizing (high-LET) radiations is qualitatively, as well as quantitatively, different from that which predominates for low-LET radiations. Comparisons of radiation track structure with observed biological effects of the radiations allow hypotheses to be developed as to the nature of these different types of damage. That associated with low-LET radiations seems consistent with what is known about DNA double-strand breaks (dsb). It is produced predominantly by a localized cluster of ionizations within a single electron 'track end' either by direct action on the DNA or in conjunction with closely-associated molecules. The characteristic high-LET damage is somewhat larger in number of ionizations and spatial extent and therefore presumably also in molecular complexity. It is suggested that the total spectrum of initial damage be categorized into four classes; in addition to the above two this would include on the one extreme sparse isolated ionizations, which may lead to very simple products that are of limited biological relevance, and on the other extreme very large and relatively rare events which are uniquely achievable by some high-LET radiations, such as alpha-particles, but not at all by low-LET radiations. These biophysical considerations pose a challenge to radiation chemistry studies to consider the chemical consequences of highly localized clusters of initial ionizations and excitations in or very near to DNA, and to biochemistry to consider classes of damage involving DNA (and perhaps associated molecules) of greater complexity than the simplest dsb.

Cells↗

PubMed1993

Inactivation and mutation induction in V79 cells by low energy protons: re-evaluation of the results at the LNL facility.

During the upgrading of the radiobiological facility at the Laboratori Nazionali di Legnaro (LNL) we found that uncorrected values of the proton energy were used in the past. This circumstance prompted us to perform the re-evaluation of the physical parameters for all the proton beams used in our previous radiobiological investigations (Belli et al. 1987) and, subsequently, the re-evaluation of all our previous dose-response curves for inactivation and mutation induction (Belli et al. 1989, 1991). This re-evaluation leads to significant changes in the dose-response curves and in the RBE-LET relationships only at the two lowest energies (highest LET) used. These two points are not reliable for the identification of a peak in RBE-LET relationship for cell inactivation. In spite of that, the extent of the changes is not such as to modify the general conclusion previously drawn, pointing out that there is a LET range where protons are more effective than alpha-particles.

Animals↗

PubMed1993

Myeloid leukaemia and osteosarcoma in CBA/H mice given 224Ra.

Four groups of 400 12-week-old CBA/H mice were injected i.p. with 69, 139, 280 and 550 Bqg-1 224Ra. A further group of 400 mice were injected i.p. with diluting solution only. The mice were then allowed unrestricted access to food and water until they died or were killed. 53 cases of myeloid leukaemia and 22 cases of osteosarcoma were confirmed in the 2000 mice injected, and for both tumour types direct relationships were shown to exist between the amount of 224Ra administered and the incidence of tumours. It is concluded that mouse is at a greater risk from myeloid leukaemia than from osteosarcoma in the region of administered 224Ra below that which causes a maximum yield of osteosarcoma. These results are discussed in the light of the present acceptance of osteosarcoma as the major risk to man from bone-seeking alpha-particle emitters.

Animals↗

PubMed1994

Chromosomal instability and alterations of telomeric repeats in irradiated human fibroblasts.

In recent years, evidence has been presented suggesting that genomic instability can appear several generations after cellular exposure to radiations. Kadhim et al. (1992) have shown that irradiation by alpha-particles of Pu238 (LET = 120 keV/microns) induce a transmissible instability in mouse haematopoietic cells. Working with human dermis fibroblasts irradiated by heavy ions in a large range of LETs (386-13,600 keV/microns), we demonstrated that an instability could also be acquired by human cells and that particular chromosomes (13, 16, 1) were recurrently involved in telomeric associations (Sabatier et al. 1992). This instability resulted in specific chromosome imbalances and in a particular monosomy 13 (Martins et al. 1993). In this study, we wanted to determine whether telomeres are shortened with the appearance of the chromosomal instability. Our results show no drastic shortening of the mean length of telomeres by Southern blot. By in situ hybridization we are looking to see if chromosomes specifically involved in instability have alterations of the telomeres. We have observed large variations of the hybridization signal of individual telomeres with no telomeric sequences detectable at the junction of end to end associations.

Cell Transformation, Neoplastic↗

PubMed1995

Delayed chromosomal instability in human T-lymphocyte clones exposed to ionizing radiation.

Recent studies have demonstrated that cells which survive alpha-particle and X-ray exposure may show chromosomal instability, i.e. they continue to develop chromosomal aberrations at an increased frequency for many division cycles after the exposure. To characterize this delayed response, we carried out repeated karyotype analyses of X-irradiated T-lymphocytes during clonal expansion in vitro. Human peripheral blood lymphocytes were obtained from a healthy donor and exposed to 3-Gy X-irradiation. Cell survival, estimated by a cell cloning assay, was 5%. Non-irradiated, control cells were studied in parallel. Monoclonal cell lines were established using the T-cell cloning procedure. G-band karyotype analyses were carried out at several intervals during expansion of the clones for up to 2 months. The irradiated clones did not differ from the control clones with regard to growth rate or cytometric DNA profile. Non-irradiated cell clones showed a normal karyotype, with < 10% of sporadic, non-clonal chromosome and chromatid breaks. In the irradiated clones, the karyotypes showed different (sub)clonal chromosome rearrangements, which developed successively during the cultivation time. In addition to these karyotypic abnormalities, > 20% of the cells in these clones had sporadic, non-clonal chromosome aberrations, and there was a tendency of increasing frequency of such aberrations by length of cultivation. Thus, two types of radiation-induced chromosomal instability were observed; (sub)clonal karyotypic abnormalities and sporadic, non-clonal chromosome aberrations. The frequency and kinetics by which these alterations occur in the progeny of X-irradiated T-cells suggest that they arise through different pathways, and argue against their causation by mutation or persistent DNA damage.

Cell Division↗

PubMed1997

A Monte Carlo calculation of cell inactivation by light ions.

This study simulates the exposure of V79 Chinese hamster fibroblasts to low-energy protons, deuterons and alpha-particles in the LET range 10-200 keV/microm. The starting assumption is that the induction of clustered lesions in DNA is a fundamental step for cell inactivation. A non-homogeneous cell population was simulated by a computer program, using as input measured morphological parameters reported in the literature. Variations in the number of traversals through each cell of the population and in the length of the traversal, depending on actual nuclear thickness and position of the traversal, the energy spread of the incident beam, and the change of LET along the tracks were included in the simulation. Microdosimetric spectra were computed and compared with spectra obtained neglecting particle slowing-down and stochastic aspects of cell morphology. Simulated cell survival was estimated under the assumption that surviving cells are those with no clustered DNA lesions or no passages. The main features of experimental RBE versus LET and particle type were reproduced by the simulations. The influence of stochastic aspects of target-cell morphology and of the energy of the incident particles on survival were investigated under different assumptions about the correlation between morphological parameters. Results support the hypothesis of a relevant role of clustered DNA damage in cell killing and point out the importance of target-cell morphology and its variability in beam dosimetry and computer simulations of low-energy particle radiation effects.

Animals↗

PubMed1998

Repair of radiation-induced DNA double-strand breaks in human fibroblasts is consistent with a continuous spectrum of repair probability.

PURPOSE: To propose a novel interpretation of DNA double-strand break (dsb) repair based on the distribution of energy micro-deposition. MATERIALS AND METHODS: Double-strand break repair curves were studied either after irradiation at 4 degrees C or at 37 degrees C (low dose rate). Two human fibroblast cell lines were used: a control line, HF19, and an ataxia telangiectasia repair-deficient line, AT5BI. Irradiations were made with gamma-rays or alpha-particles (241Am). Repair data were fitted by the variable repair half-time (VRHT) model. Assuming that each dsb has its own inherent repair half-time (IRHT) and that the VRHT is the average of the IRHT at any time during repair, the distribution of the IRHT was calculated. RESULTS: At the end of the irradiation, the distribution was a continuous asymmetric curve with a maximum of dsb having a short IRHT. After 1 h of repair, the curve became bell-shaped. There is a striking similarity between the distribution of dsb repair half-times and that of energy micro-deposition described by Goodhead et al. (1993). CONCLUSION: This similarity suggests a possible causal relationship between the energy density deposition and the repair rate or the probability of dsb repair.

Americium↗

PubMed1998

Technical report: Cell thickness measurements by confocal fluorescence microscopy on C3H10T1/2 and V79 cells.

Measurements of C3H10T1/2 and V79 cell thickness were performed on living cells by confocal laser fluorescence microscopy. Thickness distributions are reported for cells growing as a monolayer (on mylar and glass) and suspended in their medium. Mean values for cells grown on mylar (corrected for refractive index effects) are 2.9 +/- 0.6 and 6.1 +/- 1.0 microm for C3H10T1/2 and V79 cells respectively. Mean values of the diameters of cells suspended in their medium are 13.0 +/- 1.6 and 9.3 +/- 1.4 microm for C3H10T1/2 and V79 respectively. Knowledge of cell thickness, as irradiated, is of central relevance for studying the relative biological effectiveness of low energy, poorly penetrating radiations. It can be concluded, from the measured cell thickness distributions, that with C3H10T1/2 cells grown on mylar, the LET variation through the whole cell is within 20% for protons and alpha-particles with energies down to 0.6 and 2.5 MeV respectively. From a comparison with thickness values reported in the literature for living or fixed embedded cells growing on plastic substrate, mean values between 2.4 and 3.4 microm and between 6 and 7.5 microm could be assumed for C3H10T1/2 cells and for the most widely used V79 cell lines respectively.

Animals↗

PubMed1999

Increased exposure to pollutant aerosols under high voltage power lines.

PURPOSE: To assess increased exposure to airborne pollutants near power lines by investigating theoretically and experimentally the behaviour of 222Rn decay product marker aerosols in the 50 Hz electric field under power lines. MATERIALS AND METHODS: The behaviour of aerosols in outdoor air including those carrying 222Rn decay products was modelled theoretically in the presence of an AC field. TASTRAK alpha-particle spectroscopy was used to characterize 218Po and 214Po aerosols outdoors. Sampling points were chosen along a line at right angles up to 200 m from a number of high voltage power (transmission) lines. Each sampling point comprised an arrangement of mutually orthogonal TASTRAK detectors. Exposures were carried out at different power line locations in various weather conditions. RESULTS: The model predicts a two- to three-fold increase in deposition of aerosols on spherical surfaces mimicking the human head under high voltage power lines. Experimental measurements using detectors mounted on grounded metal spheres showed an enhanced deposition of both 218Po and 214Po aerosols. Enhanced 218Po deposition on 400 kV lines ranged from 1.96+/-0.15 to 2.86+/-0.32. Enhanced 214Po deposition on 275 kV and 132 kV lines were 1.43+/-0.07 and 1.11+/-0.21, respectively, where the latter value was not significant. CONCLUSIONS: The observations demonstrate a mode of increased exposure to pollutant aerosols under high voltage power lines by increased deposition on the body. The total (indoor + outdoor) 218Po and 214Po dose to the basal layer of facial skin is estimated to be increased by between 1.2 and 2.0 for 10% of time spent outdoors under high voltage power lines.

Aerosols↗

PubMed1999

RBE for carbon track-segment irradiation in cell lines of differing repair capacity.

PURPOSE: The LET position of the RBE maximum and its dependence on the cellular repair capacity was determined for carbon ions. Hamster cell lines of differing repair capacity were irradiated with monoenergetic carbon ions. RBE values for cell inactivation at different survival levels were determined and the differences in the RBE-LET patterns were compared with the individual sensitivity to photon irradiation of the different cell lines. MATERIAL AND METHODS: Three hamster cell lines, the wild-type cell lines V79 and CHO-K1 and the radiosensitive CHO mutant xrs5, were irradiated with carbon ions of different energies (2.4-266.4 MeV/u) and LET values (13.7-482.7 keV/microm) and inactivation data were measured in comparison to 250 kV x-rays. RESULTS: For the repair-proficient cell lines a RBE maximum was found at LET values between 150 and 200 keV/microm. For the repair-deficient cell line the RBE failed to show a maximum and decreased continuously for LET values above 100 keV/microm. CONCLUSIONS: The carbon RBE LET relationship for inactivation is shifted to higher LET values compared with protons and alpha-particles. RBE correlated with the repair capacity of the cells.

Animals↗

PubMedDate not supplied

Boron-loaded liposomes in the treatment of hepatic metastases: preliminary investigation by autoradiography analysis.

Boronophenylalanine (BPA)-loaded conventional and stabilized liposomes were prepared by the reversed phase evaporation method to treat liver metastases by boron neutron capture therapy. Conventional vesicles were composed of phosphatidylcholine and cholesterol, molar ratio 1:1. To obtain stealth liposomes, GM1 or PEG were included in the lipidic bilayer at a concentration of 6.67 or 5 mol%, respectively. Large unilamellar vesicles were formulated encapsulating BPA in the liposome aqueous compartment as a complex with fructose; BPA free base also was embedded into the lipidic bilayer. In vivo experiments were carried out after intravenous injection of liposome suspensions in BD-IX strain rats in which liver metastases had been induced. Alpha particle spectroscopy associated with histological analysis was performed to visualize boron spatial distribution in liver. Simultaneously, tissue boron concentrations were determined using inductively coupled plasma-mass spectroscopy. Results showed that PEG-modified liposomes accumulated boron in therapeutic concentrations (> 30 micrograms boron/g tissue) in metastatic tissue. The PEG-liposomes could be further explored in enhancing boron delivery to tumor cells.

Animals↗

PubMed2004

How to study boron biodistribution in liver metastases from colorectal cancer.

The purpose of this study was to evaluate boron distribution for a safe and effective BNCT (Boron Neutron Capture Therapy) of liver metastases. Samples both from healthy and tumour liver parenchyma were analysed, after i.v. boron administration, by: alpha particles counting under neutron irradiation; morphological analysis by standard haematoxylin-eosin staining; neutron autoradiography. Our method was unaffected by the cytological heterogeneity inside tumour nodules; it demonstrated selective boron distribution in tumour tissue and predicted estimated mean therapeutic doses in tumour and safety doses in healthy tissue. The time interval for efficient BNCT was 2 to 4 hours after i.v. boron administration.

Animals↗

PubMed2006

A combined analysis of North American case-control studies of residential radon and lung cancer.

Cohort studies have consistently shown underground miners exposed to high levels of radon to be at excess risk of lung cancer, and extrapolations based on those results indicate that residential radon may be responsible for nearly 10-15% of all lung cancer deaths per year in the United States. However, case-control studies of residential radon and lung cancer have provided ambiguous evidence of radon lung cancer risks. Regardless, alpha-particle emissions from the short-lived radioactive radon decay products can damage cellular DNA. The possibility that a demonstrated lung carcinogen may be present in large numbers of homes raises a serious public health concern. Thus, a systematic analysis of pooled data from all North American residential radon studies was undertaken to provide a more direct characterization of the public health risk posed by prolonged radon exposure. To evaluate the risk associated with prolonged residential radon exposure, a combined analysis of the primary data from seven large scale case-control studies of residential radon and lung cancer risk was conducted. The combined data set included a total of 4081 cases and 5281 controls, representing the largest aggregation of data on residential radon and lung cancer conducted to date. Residential radon concentrations were determined primarily by a-track detectors placed in the living areas of homes of the study subjects in order to obtain an integrated 1-yr average radon concentration in indoor air. Conditional likelihood regression was used to estimate the excess risk of lung cancer due to residential radon exposure, with adjustment for attained age, sex, study, smoking factors, residential mobility, and completeness of radon measurements. Although the main analyses were based on the combined data set as a whole, we also considered subsets of the data considered to have more accurate radon dosimetry. This included a subset of the data involving 3662 cases and 4966 controls with a-track radon measurements within the exposure time window (ETW) 5-30 yr prior to the index date considered previously by Krewski et al. (2005). Additional restrictions focused on subjects for which a greater proportion of the ETW was covered by measured rather than imputed radon concentrations, and on subjects who occupied at most two residences. The estimated odds ratio (OR) of lung cancer generally increased with radon concentration. The OR trend was consistent with linearity (p = .10), and the excess OR (EOR) was 0.10 per Bq/m3 with 95% confidence limits (-0.01, 0.26). For the subset of the data considered previously by Krewski et al. (2005), the EOR was 0.11 (0.00, 0.28). Further limiting subjects based on our criteria (residential stability and completeness of radon monitoring) expected to improve radon dosimetry led to increased estimates of the EOR. For example, for subjects who had resided in only one or two houses in the 5-30 ETW and who had a-track radon measurements for at least 20 yr of this 25-yr period, the EOR was 0.18 (0.02, 0.43) per 100 Bq/m3. Both estimates are compatible with the EOR of 0.12 (0.02, 0.25) per 100 Bq/m3 predicted by downward extrapolation of the miner data. Collectively, these results provide direct evidence of an association between residential radon and lung cancer risk, a finding predicted by extrapolation of results from occupational studies of radon-exposed underground miners.

Adult↗

PubMed1957

Electron microscopic observations of amoeba proteus in growth and inanition.

Electron microscopic observations have been made on growing and dividing specimens of Amoeba proteus and also on starving animals. Structures presumably corresponding to the mitochondria, alpha particles, vacuoles, and Golgi material are described. A new entity, designated as a foamy particle, is noted. Descriptions are given of the cytoplasmic and nuclear membranes. During division the inner, thick nuclear membrane component is seen to vanish and the outer membrane persist. Measurements suggest a gradual reappearance of the inner component with growth. Starving animals show a loss of cytoplasmic granularity and an increase in the electron density of mitochondria, presumably due to lipide accumulation.

Amoeba↗

PubMed1977

Aspects of the dosimetry of alpha-emitting radionuclides in bone with particular emphasis on 226Ra and 239Pu.

The dosimetry of alpha-emitting radionuclides in bone is discussed. Results are presented for average dose rates to tissues close to endosteal surfaces and to haematopoietic bone marrow from thin plane sources of radionuclides buried to different depths in bone and emitting alpha-particles with energies in the range 3-8 MeV. These results are used to demonstrate that on an activity basis 239Pu is unlikely to be more than fifteen times as toxic as 226Ra with respect to osteosarcoma and leukaemia induction in man.

Animals↗