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At least 91 records · Page 5
All sourcesNASA NTRSDOE OSTI
NASA NTRS2011

Step-by-Step Simulation of Radiation Chemistry Using Green Functions for Diffusion-Influenced Reactions

Radiolytic species are formed approximately 1 ps after the passage of ionizing radiation through matter. After their formation, they diffuse and chemically react with other radiolytic species and neighboring biological molecules, leading to various oxidative damage. Therefore, the simulation of radiation chemistry is of considerable importance to understand how radiolytic species damage biological molecules [1]. The step-by-step simulation of chemical reactions is difficult, because the radiolytic species are distributed non-homogeneously in the medium. Consequently, computational approaches based on Green functions for diffusion-influenced reactions should be used [2]. Recently, Green functions for more complex type of reactions have been published [3-4]. We have developed exact random variate generators of these Green functions [5], which will allow us to use them in radiation chemistry codes. Moreover, simulating chemistry using the Green functions is which is computationally very demanding, because the probabilities of reactions between each pair of particles should be evaluated at each timestep [2]. This kind of problem is well adapted for General Purpose Graphic Processing Units (GPGPU), which can handle a large number of similar calculations simultaneously. These new developments will allow us to include more complex reactions in chemistry codes, and to improve the calculation time. This code should be of importance to link radiation track structure simulations and DNA damage models.

Plante, Ianik↗
NASA NTRSDate not supplied

AMMPER: Agent-based Model for Microbial Populations Exposed to Radiation

Exposure of microbial populations to galactic cosmic radiation (GCR) in the deep-space radiation environment may lead to intracellular damage that compromises the ability of cells to repair and replicate. While simulation programs of deep-space radiation do exist, they focus primarily on single-cell damage, rather than population-wide effects. In this work, a new application and graphical user interface, Agent-Based Model for Microbial Populations Exposed to Radiation (AMMPER) is presented, which simulates the effects of proton-based GCR on Saccharomyces cerevisiae population growth. AMMPER consists of a 50x50x50 µm simulation space, analogous to an aqueous culture medium with non-limiting nutrient and pH buffering, in a microwell plate or microfluidic culture card. This model utilizes Relativistic Ion Tracks (RITRACKS) to create detailed track structures of the radiation traversals. AMMPER then calculates the radiation dose present at each cell, and subsequently determines the damage (chromosomal aberrations, oxidative stress, etc.) and resulting loss of cell viability from both primary and secondary radiative effects. Through implementing cell replication, repair, damage, and death, the effect of radiation exposure on the population growth can be determined. With AMMPER, long-duration effects of the deep space environment on entire populations can be determined and used to assess the feasibility of sustaining life in space.

Amrita Singh↗
NASA NTRS1999

Future Radiation Damage in Space due to South Atlantic Anomaly

Predictions of radiation damage for Low Earth Orbit (LEO) satellites now use semi-empirical models developed from prior satellite data. From these models it is clear that the low field strength of the South Atlantic Anomaly (SAA) controls where the maximum radiation damage occurs. One may make an estimate of future radiation damage to LEO spacecraft if one can predict the future of the SAA. Although reliable maps of the geomagnetic field strength and its secular change have only been made in the last few decades, certain geomagnetic observatories in South America and Africa have recorded the geomagnetic field for a much longer time. These observatories show that the present geomagnetic field change has persisted for more than 100 years. In spite of the fact that a few observatories have shown sudden changes in secular variation, those around the SAA have shown a stable secular variation. Assuming that this will continue for the next 50 to 100 years one can show that the SAA will expand to cover most of the South Atlantic Ocean and will become much weaker. This will greatly intensify the radiation hazard in LEO, put significant new limitations on radiation-hardened hardware, severely restrict the length of time that humans can remain in orbit, and materially change the configuration of the radiation belts.

Heirtzler, J. R.↗
NASA NTRSDate not supplied

Neuroimmune Responses to Space Radiation

One of the main health risks in human deep space exploration is central nervous system (CNS) damage by ionizing radiation due to exposure to galactic cosmic rays (GCRs). In animal models, irradiation with simulated GCRs or their components has been shown to cause neurodegeneration and neuroinflammation associated with cognitive and behavioral dysfunction. The extent of CNS damage is partially mediated by the blood-brain barrier (BBB), which regulates the interaction between CNS and systemic responses to stressors in the rest of the body. The main cellular regulators of BBB permeability are astrocytes, which also modulate neuronal death, neuroinflammation and oxidative stress. However, studies on BBB and astrocyte functions in regulating CNS responses to ionizing radiation have been limited, especially in human tissue/organ analogs. Therefore, we developed a high-throughput 3D organ-on-a-chip system to study human CNS and BBB impairments caused by deep space radiation. We investigated both immediate and delayed CNS responses to major GCR components: 600MeV/n 56Fe ions. We observed ionizing radiation-mediated dose-dependent increases in BBB permeability that was exacerbated by astrocyte presence and accompanied by altered cytokine expression including interleukin-1 receptor alpha downregulation, and increased oxidative stress. In particular, 600MeV/n 56Fe particle irradiation selectively increased damage and blood-brain barrier permeability only in models that contained astrocytes in addition to endothelial cells, indicating astrocytes as a particularly radiosensitive component of the CNS that could therefore be a suitable a target for neuroprotection. Future studies will compare human and mouse CNS model responses to simulated GCRs and evaluate the induction of an anti-inflammatory phenotype in astrocytes as a potential countermeasure. Furthermore, in our lab we have been exploring the individual variability, genomic associations and secreted biomarkers of responses to space radiation, which could eventually be combined to address personalized CNS health risk and develop individual countermeasures. Ultimately, we aim to expand upon these results to uncover novel cellular and mechanistic targets for countermeasure development to mitigate human CNS damage in deep space exploration.

space radiation↗
NASA NTRSDate not supplied

Neuroimmune responses to space radiation

One of the main health risks in human deep space exploration is central nervous system (CNS) damage by ionizing radiation due to exposure to galactic cosmic rays (GCRs). In animal models, irradiation with simulated GCRs or their components has been shown to cause neurodegeneration and neuroinflammation associated with cognitive and behavioral dysfunction. The extent of CNS damage is partially mediated by the blood-brain barrier (BBB), which regulates the interaction between CNS and systemic responses to stressors in the rest of the body. The main cellular regulators of BBB permeability are astrocytes, which also modulate neuronal death, neuroinflammation and oxidative stress. However, studies on BBB and astrocyte functions in regulating CNS responses to ionizing radiation have been limited, especially in human tissue/organ analogs. Therefore, we developed a high-throughput 3D organ-on-a-chip system to study human CNS and BBB impairments caused by deep space radiation. We investigated both immediate and delayed CNS responses to major GCR components: 0.3-0.8Gy 600MeV/n 56Fe ions; as well as to 0.5-1Gy X-rays. We observed ionizing radiation-mediated increases in BBB permeability that was exacerbated by astrocyte presence and accompanied by damage to endothelial cells and tight junctions, altered cytokine expression including TNFalpha upregulation, and increased oxidative stress. In particular, 600MeV/n 56Fe particle irradiation selectively induced astrocyte damage and increased blood-brain barrier permeability only in models that contained astrocytes in addition to endothelial cells, indicating astrocytes as a particularly radiosensitive component of the CNS that could therefore be a suitable a target for neuroprotection. Future studies will compare human and mouse CNS model responses to simulated GCRs and evaluate the induction of an anti-inflammatory phenotype in astrocytes as a potential countermeasure. Furthermore, in our lab we have been exploring the individual variability, genomic associations and secreted biomarkers of responses to space radiation, which could eventually be combined to address personalized CNS health risk and develop individual countermeasures. Ultimately, we aim to expand upon these results to uncover novel cellular and mechanistic targets for countermeasure development to mitigate human CNS damage in deep space exploration.

space radiation↗
NASA NTRS2006

A Strategy to Safely Live and Work in the Space Radiation Environment

The goal of the National Aeronautics and Space Agency and the Space Radiation Project is to ensure that astronauts can safely live and work in the space radiation environment. The space radiation environment poses both acute and chronic risks to crew health and safety, but unlike some other aspects of space travel, space radiation exposure has clinically relevant implications for the lifetime of the crew. The term safely means that risks are sufficiently understood such that acceptable limits on mission, post-mission and multi-mission consequences (for example, excess lifetime fatal cancer risk) can be defined. The Space Radiation Project strategy has several elements. The first element is to use a peer-reviewed research program to increase our mechanistic knowledge and genetic capabilities to develop tools for individual risk projection, thereby reducing our dependency on epidemiological data and population-based risk assessment. The second element is to use the NASA Space Radiation Laboratory to provide a ground-based facility to study the understanding of health effects/mechanisms of damage from space radiation exposure and the development and validation of biological models of risk, as well as methods for extrapolation to human risk. The third element is a risk modeling effort that integrates the results from research efforts into models of human risk to reduce uncertainties in predicting risk of carcinogenesis, central nervous system damage, degenerative tissue disease, and acute radiation effects. To understand the biological basis for risk, we must also understand the physical aspects of the crew environment. Thus the fourth element develops computer codes to predict radiation transport properties, evaluate integrated shielding technologies and provide design optimization recommendations for the design of human space systems. Understanding the risks and determining methods to mitigate the risks are keys to a successful radiation protection strategy.

Corbin, Barbara J.↗
NASA NTRSDate not supplied

Effects Of Five-Ion Galactic Cosmic Radiation Simulation On Immune Function, Brain, And Behavior In Male And Female Mice

Exposure to galactic cosmic radiation is a principal consideration of spaceflight missions, and with upcoming missions to the Moon and Mars, it is increasingly imperative to elucidate the effects of space travel beyond the lower Earth orbit. Additionally, with the first female astronaut to soon travel to the Moon there is a strong need to understand the biological sex differences to adaptation to the deep space environment. While the effects of spaceflight on the nervous system are not fully known, studies in animal models have shown that exposure to ionizing radiation can cause neuronal damage and lead to downstream cognitive and behavioral deficits. To simulate the type of radiation exposure occurring during spaceflight, model organisms can be exposed to relevant doses via Five-Ion Galactic Cosmic Radiation Simulation at the NASA National Space Radiation Laboratory at Brookhaven National Laboratory. We have investigated the neurobehavioral responses to space environment-like radiation exposure. Male and female 23–24-week-old mice (age-matched to average astronaut age) were exposed to 5, 15 and 50 cGy. Following exposure, immune, brain and behavioral (sensorimotor, risk-taking and cognitive) measures were acquired at ‘Acute’ (IR+24hrs, IR+72hrs), ‘Intermediate’ (IR+14 days) and ‘Delayed’ (IR+28 to IR+124 days) to inform biological responses anticipated during a transit to Moon and Mars. There were pronounced sex differences observed in all outcome measurements, while very few radiation induced effects were observed. Those dose effects that were observed were primarily in cytokine expression and less so in behavioral measurements. Further studies will investigate if radiation, microgravity and social isolation combine synergistically to trigger an oxidative stress response that alters immune homeostasis, brain structure/function, and neurobehavioral/cognitive performance, ultimately to characterize risks and identify appropriate countermeasures in both women and men in anticipation of future deep space missions.

Stephanie Puukila↗
NASA NTRS1996

Clusters of DNA induced by ionizing radiation: formation of short DNA fragments. I. Theoretical modeling

We have developed a general theoretical model for the interaction of ionizing radiation with chromatin. Chromatin is modeled as a 30-nm-diameter solenoidal fiber comprised of 20 turns of nucleosomes, 6 nucleosomes per turn. Charged-particle tracks are modeled by partitioning the energy deposition between primary track core, resulting from glancing collisions with 100 eV or less per event, and delta rays due to knock-on collisions involving energy transfers >100 eV. A Monte Carlo simulation incorporates damages due to the following molecular mechanisms: (1) ionization of water molecules leading to the formation of OH, H, eaq, etc.; (2) OH attack on sugar molecules leading to strand breaks: (3) OH attack on bases; (4) direct ionization of the sugar molecules leading to strand breaks; (5) direct ionization of the bases. Our calculations predict significant clustering of damage both locally, over regions up to 40 bp and over regions extending to several kilobase pairs. A characteristic feature of the regional damage predicted by our model is the production of short fragments of DNA associated with multiple nearby strand breaks. The shapes of the spectra of DNA fragment lengths depend on the symmetries or approximate symmetries of the chromatin structure. Such fragments have subsequently been detected experimentally and are reported in an accompanying paper (B. Rydberg, Radiat, Res. 145, 200-209, 1996) after exposure to both high- and low-LET radiation. The overall measured yields agree well quantitatively with the theoretical predictions. Our theoretical results predict the existence of a strong peak at about 85 bp, which represents the revolution period about the nucleosome. Other peaks at multiples of about 1,000 bp correspond to the periodicity of the particular solenoid model of chromatin used in these calculations. Theoretical results in combination with experimental data on fragmentation spectra may help determine the consensus or average structure of the chromatin fibers in mammalian DNA.

Non-NASA Center↗
NASA NTRS2014

Transgenic Mouse Model for Reducing Oxidative Damage in Bone

Exposure to musculoskeletal disuse and radiation result in bone loss; we hypothesized that these catabolic treatments cause excess reactive oxygen species (ROS), and thereby alter the tight balance between bone resorption by osteoclasts and bone formation by osteoblasts, culminating in bone loss. To test this, we used transgenic mice which over-express the human gene for catalase, targeted to mitochondria (MCAT). Catalase is an anti-oxidant that converts the ROS hydrogen peroxide into water and oxygen. MCAT mice were shown previously to display reduced mitochondrial oxidative stress and radiosensitivity of the CNS compared to wild type controls (WT). As expected, MCAT mice expressed the transgene in skeletal tissue, and in marrow-derived osteoblasts and osteoclast precursors cultured ex vivo, and also showed greater catalase activity compared to wildtype (WT) mice (3-6 fold). Colony expansion in marrow cells cultured under osteoblastogenic conditions was 2-fold greater in the MCAT mice compared to WT mice, while the extent of mineralization was unaffected. MCAT mice had slightly longer tibiae than WT mice (2%, P less than 0.01), although cortical bone area was slightly lower in MCAT mice than WT mice (10%, p=0.09). To challenge the skeletal system, mice were treated by exposure to combined disuse (2 wk Hindlimb Unloading) and total body irradiation Cs(137) (2 Gy, 0.8 Gy/min), then bone parameters were analyzed by 2-factor ANOVA to detect possible interaction effects. Treatment caused a 2-fold increase (p=0.015) in malondialdehyde levels of bone tissue (ELISA) in WT mice, but had no effect in MCAT mice. These findings indicate that the transgene conferred protection from oxidative damage caused by treatment. Unexpected differences between WT and MCAT mice emerged in skeletal responses to treatment.. In WT mice, treatment did not alter osteoblastogenesis, cortical bone area, moment of inertia, or bone perimeter, whereas in MCAT mice, treatment increased these parameters. Taken together, this typically catabolic treatment (disuse and irradiation) appeared to stimulate cortical expansion in MCAT mice but not WT mice. In conclusion, these results reveal the importance of mitochondrial ROS generation in skeletal remodeling and show that MCAT mice provide a useful animal model for bone studies.

trandgenic↗
NASA NTRS2009

Development of a GCR Event-based Risk Model

A goal at NASA is to develop event-based systems biology models of space radiation risks that will replace the current dose-based empirical models. Complex and varied biochemical signaling processes transmit the initial DNA and oxidative damage from space radiation into cellular and tissue responses. Mis-repaired damage or aberrant signals can lead to genomic instability, persistent oxidative stress or inflammation, which are causative of cancer and CNS risks. Protective signaling through adaptive responses or cell repopulation is also possible. We are developing a computational simulation approach to galactic cosmic ray (GCR) effects that is based on biological events rather than average quantities such as dose, fluence, or dose equivalent. The goal of the GCR Event-based Risk Model (GERMcode) is to provide a simulation tool to describe and integrate physical and biological events into stochastic models of space radiation risks. We used the quantum multiple scattering model of heavy ion fragmentation (QMSFRG) and well known energy loss processes to develop a stochastic Monte-Carlo based model of GCR transport in spacecraft shielding and tissue. We validated the accuracy of the model by comparing to physical data from the NASA Space Radiation Laboratory (NSRL). Our simulation approach allows us to time-tag each GCR proton or heavy ion interaction in tissue including correlated secondary ions often of high multiplicity. Conventional space radiation risk assessment employs average quantities, and assumes linearity and additivity of responses over the complete range of GCR charge and energies. To investigate possible deviations from these assumptions, we studied several biological response pathway models of varying induction and relaxation times including the ATM, TGF -Smad, and WNT signaling pathways. We then considered small volumes of interacting cells and the time-dependent biophysical events that the GCR would produce within these tissue volumes to estimate how GCR event rates mapped to biological signaling induction and relaxation times. We considered several hypotheses related to signaling and cancer risk, and then performed simulations for conditions where aberrant or adaptive signaling would occur on long-duration space mission. Our results do not support the conventional assumptions of dose, linearity and additivity. A discussion on how event-based systems biology models, which focus on biological signaling as the mechanism to propagate damage or adaptation, can be further developed for cancer and CNS space radiation risk projections is given.

Cucinotta, Francis A.↗
NASA NTRS1994

Neuritogenesis: A model for space radiation effects on the central nervous system

Pivotal to the astronauts' functional integrity and survival during long space flights are the strategies to deal with space radiations. The majority of the cellular studies in this area emphasize simple endpoints such as growth related events which, although useful to understand the nature of primary cell injury, have poor predictive value for extrapolation to more complex tissues such as the central nervous system (CNS). In order to assess the radiation damage on neural cell populations, we developed an in vitro model in which neuronal differentiation, neurite extension, and synaptogenesis occur under controlled conditions. The model exploits chick embryo neural explants to study the effects of radiations on neuritogenesis. In addition, neurobiological problems associated with long-term space flights are discussed.

Vazquez, M. E.↗
NASA NTRS1983

Lunar and Planetary Science Conference, 13th, Houston, TX, March 15-19, 1982, Proceedings. Part 2

The second part of the proceedings of the Thirteenth Lunar and Planetary Science Conference considers sedimentary processes and crustal cycling on Venus, a model for the formation of the earth's core, evidence of resurfacing in the lunar nearside highlands, the geology of Tethys, thermal stresses in planetary elastic lithospheres, the petrology and comparative thermal and mechanical histories of clasts in breccia 62236, lunar paleointensity data and its implications for the origin of lunar magnetism, and a model for the accumulation of solar wind radiation damage effects in lunar dust grains. Also discussed are fluid inclusions in stony meteorites, nuclear track and compositional studies of olivines in CI and CM chondrites, the impact of an asteroid or comet in the ocean and the extinction of terrestrial life, cooling rates for glass-containing lunar compositions, and the homogeneity of lava flows.

Boynton, W. V.↗
NASA NTRS2009

KSC Tech Transfer News, Volume 2, No. 2

This issue contains articles about: (1) the Innovative Partnerships Program (IPP) and the manager of the program, Alexis Hongamen, (2) New Technology Report (NTR) on a Monte Carlo Simulation to Estimate the Likelihood of Direct Lightning Strikes, (3) Kennedy Space Center's Applied Physics Lab, (4) a virtual ruler that is used for many applications, (5) a portable device that finds low-level leaks, (6) a sun-shield, that supports in-space cryogenic propellant storage, (7) lunar dust modeling software, (8) space based monitoring of radiation damage to DNA, (9) the use of light-emitting diode (LED) arrays vegetable production system, (10) Dust Tolerant Intelligent Electrical Connection Systems, (11) Ice Detection Camera System Upgrade, (12) Repair Techniques for Composite Structures, (13) Cryogenic Orbital Testbed, and (14) copyright protection.

Makufka, David↗
NASA NTRS2001

Comparison of F ratios generated from interphase and metaphase chromosome damage induced by high doses of low- and high-LET radiation

Although biophysical models predict a difference in the ratio of interchromosomal to intrachromosomal interarm exchanges (F ratio) for low- and high-LET radiations, few experimental data support this prediction. However, the F ratios in experiments to date have been generated using data on chromosome aberrations in samples collected at the first postirradiation mitosis, which may not be indicative of the aberrations formed in interphase after exposure to high-LET radiations. In the present study, we exposed human lymphocytes in vitro to 2 and 5 Gy of gamma rays and 3 Gy of 1 GeV/nucleon iron ions (LET = 140 keV/micrometer), stimulated the cells to grow with phytohemagglutinin (PHA), and collected the condensed chromosomes after 48 h of incubation using both chemically induced premature chromosome condensation (PCC) and the conventional metaphase techniques. The PCC technique used here condenses chromosomes mostly in the G(2) phase of the cell cycle. The F ratio was calculated using data on asymmetrical chromosome aberrations in both the PCC and metaphase samples. It was found that the F ratios were similar for the samples irradiated with low- and high-LET radiation and collected at metaphase. However, for irradiated samples assayed by PCC, the F ratio was found to be 8.2 +/- 2.0 for 5 Gy gamma rays and 5.2 +/- 0.9 for 3 Gy iron ions. The distribution of the aberrations indicated that, in the PCC samples irradiated with iron ions, most of the centric rings occurred in spreads containing five or more asymmetrical aberrations. These heavily damaged cells, which were either less likely to reach mitosis or may reach mitosis at a later time, were responsible for the difference in the F ratios generated from interphase and metaphase analysis after exposure to iron ions.

NASA Discipline Radiation Health↗
NASA NTRS1994

Dose rate and repair effects on cell damage in earth orbit

Radiobiology experiments performed in space will encounter continuous exposures to the cosmic rays and fractionated exposures to trapped protons which accumulate to several hundred dose fractions in a few weeks. Using models of track structure and cellular kinetics combined with models of the radiation environment and radiation transport, we consider calculations of damage rates for cell cultures. Analysis of the role of repair mechanisms for space exposures for the endpoints of survival and transformation is emphasized.

Cucinotta, F. A.↗
NASA NTRS1971

Dependence of defect introduction on temperature and resistivity and some long-term annealing effects

The effort reported here represents data of lithium properties in bulk-silicon samples before and after irradiation for analytical information required to characterize the interactions of lithium with radiation-induced defects in silicon. A model of the damage and recovery mechanisms in irradiated-lithium-containing solar cells is developed based on making measurements of the Hall coefficient and resistivity of samples irradiated by 1-MeV electrons. Experiments on bulk samples included Hall coefficient and resistivity measurements taken as a function of: (1) bombardment temperature, (2) resistivity, (3) fluence, (4) oxygen concentration, and (5) annealing time at temperatures from 300 to 373 K.

Brucker, G. J.↗
NASA NTRS1991

InP/Ga0.47In0.53As monolithic, two-junction, three-terminal tandem solar cells

The work presented has focussed on increasing the efficiency of InP-based solar cells through the development of a high-performance InP/Ga(0.47)In(0.53)As two-junction, three-terminal monolithic tandem cell. Such a tandem is particularly suited to space applications where a radiation-hard top cell (i.e., InP) is required. Furthermore, the InP/Ga(0.47)In(0.53)As materials system is lattice matched and offers a top cell/bottom cell bandgap differential (0.60 eV at 300 K) suitable for high tandem cell efficiencies under AMO illumination. A three-terminal configuration was chosen since it allows for independent power collection from each subcell in the monolithic stack, thus minimizing the adverse impact of radiation damage on the overall tandem efficiency. Realistic computer modeling calculations predict an efficiency boost of 7 to 11 percent from the Ga(0.47)In(0.53)As bottom cell under AMO illumination (25 C) for concentration ratios in the 1 to 1000 range. Thus, practical AMO efficiencies of 25 to 32 percent appear possible with the InP/Ga(0.47)In(0.53)As tandem cell. Prototype n/p/n InP/Ga(0.47)In(0.53)As monolithic tandem cells were fabricated and tested successfully. Using an aperture to define the illuminated areas, efficiency measurements performed on a non-optimized device under standard global illumination conditions (25 C) with no antireflection coating (ARC) give 12.2 percent for the InP top cell and 3.2 percent for the Ga(0.47)In(0.53)As bottom cell, yielding an overall tandem efficiency of 15.4 percent. With an ARC, the tandem efficiency could reach approximately 22 percent global and approximately 20 percent AMO. Additional details regarding the performance of individual InP and Ga(0.47)In(0.53)As component cells, fabrication and operation of complete tandem cells and methods for improving the tandem cell performance, are also discussed.

Wanlaas, M. W.↗
NASA NTRS1996

Rejoining and misrejoining of radiation-induced chromatin breaks. II. Biophysical Model

A biophysical model for the kinetics of the formation of radiation-induced chromosome aberrations is developed to account for the recent experimental results obtained with a combination of the premature chromosome condensation (PCC) and fluorescence in situ hybridization (FISH) techniques. In this model, we consider the broken ends of DNA double-strand breaks (DSBs) to be reactant and make use of the interaction distance hypothesis. The repair/misrepair process between broken ends is suggested to consist of two steps; the first step represents the two break ends approaching each other, and the second step represents the enzymatic processes leading to DNA end-to-end rejoining. Only the second step is reflected in the kinetics observed in experiments using PCC. The model appears to be able to fit existing data for human cells. It is shown that the kinetics of the formation of chromosome aberrations can be explained by a single rate that characterizes both rejoining and misrejoining of DSBs, suggesting that repair and misrepair share the same mechanism. Fast repair (completed in minutes) in a subset of DSBs is suggested as an explanation of the complete exchanges observed with PCC in human lymphocytes immediately after irradiation. The fast repair component seems to be absent in human fibroblasts.

NASA Center JSC↗