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At least 109 records · Page 6
All sourcesNASA NTRSDOE OSTI
NASA NTRSDate not supplied

Neurovascular Outcomes of Ionizing Radiation in Human Blood-Brain Barrier Models

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: 0.15-0.5Gy 250MeV/n 4He and 0.3-0.8Gy 600MeV/n 56Fe; 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 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. 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↗
DOE OSTI2023

Ionizing Radiation Sensing with Functionalized and Copper-Coated SWCNT/PMMA Thin Film Nanocomposites

This paper studies the ionizing radiation effects on functionalized single-walled carbon nanotube (SWCNT)/poly(methyl methacrylate) (PMMA) thin-film nanocomposites [SWNT/PMMA]. The functionalized thin-film devices are made of ferrocene-doped SWCNTs, SWCNTs functionalized with carboxylic acid (COOH), and SWCNTs coated/ modified with copper. The nanocomposite was synthesized by the solution blending method and the resulting nanocomposite was spin-cast on interdigitated electrodes (IDEs). A 160 kV X-ray source was used to irradiate the thin film and changes in the electrical resistance of the nanocomposites due to X-rays were measured using a semiconductor device analyzer. Carboxylic acid functionalized and copper-coated SWCNT/PMMA nanocomposite showed a reduced response to X-rays compared to unfunctionalized SWCNT/PMMA nanocomposite. Ferrocene-doped SWCNT showed a higher sensitivity to X-rays at lower dose rates. This is in contrast to a previous study that showed that similar nanocomposites using functionalized multi-walled CNTs (MWCNTs) had demonstrated an improved response to X-rays ionizing radiation compared to unfunctionalized MWCNTs for all dose rates. Electrical measurements were also performed using the Arduino Nano microcontroller. The result showed that a relatively economical, lightweight-designed prototype radiation sensor based on SWCNT/PMMA thin-film devices could be produced by interfacing the devices with a modest microcontroller. This work also shows that by encapsulating the SWCNT/PMMA thin-film device in a plastic container, the effect of ambient humidity can be reduced and the device can still be used to detect X-ray radiation. This study further shows that the sensitivity of SWCNT to X-rays was dependent on both the functionalization of the SWCNT and the dose rate.

36 MATERIALS SCIENCE↗
NASA NTRS2019

Predicting Cancer Risk from Ionizing Radiation

The ability to predict cancer risk associated with exposure to low doses of high-LET ionizing radiation (IR) remains a challenge. Epidemiological methods lack the sensitivity and power to provide detailed risk estimates for cancer and ignore individual variance in IR sensitivity. We have hypothesized that DNA repair capacity can be used as a marker to evaluate and differentiate individual radiation sensitivity. More specifically, this work is based on the concept that the combined time-dose dependence of radiation-induced foci (RIF) of p53-binding protein 1 (53BP1) following low-LET exposure contains sufficient information to infer sensitivity to any other LET. Our hypothesis was tested in 15 different mouse strains as well as in primary human immune cells. We first approached individual ionizing radiation sensitivity in a mouse model by culturing primary skin fibroblasts extracted from 76 mice of 15 different genetic backgrounds and exposing them to HZE particles and X-rays. This work is one of the most extensive studies on the kinetics and possible genetic underpinnings of radiation-induced DNA damage and repair. Our results is in agreement with a DNA repair model we previously postulated, where nearby DNA double strand breaks (DSB) in the nucleus are brought together for more efficient repair, leading to RIF clustering. Such mechanism was evidenced by a specific dose and LET dependence of RIF numbers. Briefly, RIF quantification after low-LET X-ray exposure showed an asymptotic saturation for doses between 1 Gy and 4 Gy 4 hours post-irradiation across all 15 strains. The clustering of DSB across all strains also led to more RIF/Gy for lower LET (X-ray and 350 MeV/n Ar) than for higher LET (600 MeV/n Fe) 4 hours post-exposure. Considering the fact that the number of DSB/Gy should be independent of LET, our data suggest there are more DSB in individual RIF as the LET increases. RIF numbers for 24 and 48 hours post-exposure led to the inverse trend, with more remaining RIF/Gy for higher LET (by 600 MeV/n Fe). This result suggests cells have more difficulty resolving RIF from higher LET as they the number DSB/RIF increases. Note that for most conditions, the variance of RIF/Gy was small within individual animals of the same strain and large between strains, suggesting a strong genetics component. Furthermore, we present our preliminary data from an ongoing study on human genetic associations with IR sensitivity. To address the human variability in responses to HZE particle irradiation in a maximally comprehensive manner, we are in the process of collecting and isolating primary blood mononuclear cells from 768 healthy subjects of European descent, 18-75 years of age, 50/50 male/female distribution. We have analyzed 53BP1+ RIF formation as well as oxidative stress and cell death in primary cells from 192 subjects in response to the same HZE particles as used in mice: 600 MeV/n Fe, 350 MeV/n Ar and 350 MeV/n Si, 1.1 and 3 particles/100m2, 4 and 24 hours after irradiation. We will next complete the quantification of HZE particle-induced DNA and cellular damage in the remaining subjects and compare it to their responses to low-LET irradiation. Finally, we will perform GWAS analysis to identify human genomic associations with IR sensitivity and potential targets for biomarker development.

High-LET radiation↗
DOE OSTI2021

Exposure to ionizing radiation disrupts normal epigenetic aging in Japanese medaka

Alterations to the epigenome are a hallmark of biological aging and age-dependent patterning of the DNA methylome (“epigenetic aging”) can be modeled to produce epigenetic age predictors. Rates of epigenetic aging vary amongst individuals and correlate to the onset of age-related disease and all-cause mortality. Yet, the origins of epigenetic-to-chronological age discordance are not empirically resolved. Here, we investigate the relationship between aging, DNA methylation, and environmental exposures in Japanese medaka (Oryzias latipes). We find age-associated DNA methylation patterning enriched in genomic regions of low CpG density and that, similar to mammals, most age-related changes occur during early life. We construct an epigenetic clock capable of predicting chronological age with a mean error of 61.1 days (~8.4% of average lifespan). To test the role of environmental factors in driving epigenetic age variation, we exposed medaka to chronic, environmentally relevant doses of ionizing radiation. Because most organisms share an evolutionary history with ionizing radiation, we hypothesized that exposure would reveal fundamental insights into environment-by-epigenetic aging interactions. Radiation exposure disrupted epigenetic aging by accelerating and decelerating normal age-associated patterning and was most pronounced in cytosines that were moderately associated with age. These findings empirically demonstrate the role of DNA methylation in integrating environmental factors into aging trajectories.

60 APPLIED LIFE SCIENCES↗
NASA NTRS2003

Non-targeted and delayed effects of exposure to ionizing radiation: II. Radiation-induced genomic instability and bystander effects in vivo, clastogenic factors and transgenerational effects

The goal of this review is to summarize the evidence for non-targeted and delayed effects of exposure to ionizing radiation in vivo. Currently, human health risks associated with radiation exposures are based primarily on the assumption that the detrimental effects of radiation occur in irradiated cells. Over the years a number of non-targeted effects of radiation exposure in vivo have been described that challenge this concept. These include radiation-induced genomic instability, bystander effects, clastogenic factors produced in plasma from irradiated individuals that can cause chromosomal damage when cultured with nonirradiated cells, and transgenerational effects of parental irradiation that can manifest in the progeny. These effects pose new challenges to evaluating the risk(s) associated with radiation exposure and understanding radiation-induced carcinogenesis.

Review, Tutorial↗
NASA NTRS2003

Non-targeted and delayed effects of exposure to ionizing radiation: I. Radiation-induced genomic instability and bystander effects in vitro

A long-standing dogma in the radiation sciences is that energy from radiation must be deposited in the cell nucleus to elicit a biological effect. A number of non-targeted, delayed effects of ionizing radiation have been described that challenge this dogma and pose new challenges to evaluating potential hazards associated with radiation exposure. These effects include induced genomic instability and non-targeted bystander effects. The in vitro evidence for non-targeted effects in radiation biology will be reviewed, but the question as to how one extrapolates from these in vitro observations to the risk of radiation-induced adverse health effects such as cancer remains open.

Review, Tutorial↗
NASA NTRSDate not supplied

Neurovascular Outcomes of Ionizing Radiation in Human Blood-Brain Barrier Models

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 human neurovascular system model, based on commercially available Mimetas OrganoPlates seeded by primary human cells, to investigate the neurovascular responses to simulated deep space radiation. Using this system, we have demonstrated that 600MeV/n 56Fe irradiation leads to cellular damage and increased blood-brain barrier permeability via dysfunction of brain cells called astrocytes, which appear to be the weakest link and therefore a highly suitable countermeasure target to reduce the impact of space radiation on the blood-brain barrier. We anticipate that our results form merely the first step in ongoing development of organ models, including their adaptation for personalized risk assessment, high throughput approaches to countermeasure screening and validation, and eventual payload adaptation.

organ-on-a-chip↗
NASA NTRS1992

Ionizing radiation environment for the TOMS mission

The Total Ozone Mapping Spectrometer (TOMS) will fly on several different spacecraft, each having an orbit which is approximately polar and 800-980 km in altitude. A description is given of the computer-based tools used for characterizing the spacecraft interactions with the ionizing radiation environment in orbit and the susceptibility requirements for ionizing radiation compatibility. The peak flux from the model was used to derive the expected radiation-induced noise in the South Atlantic Anomaly for the new TOMS instruments intended to fly on Advanced Earth Observatory System and Earth Probe.

Lauriente, M.↗
NASA NTRS1999

Astronaut Exposures to Ionizing Radiation in a Lightly-Shielded Spacesuit

The normal working and living areas of the astronauts are designed to provide an acceptable level of protection against the hazards of ionizing radiation of the space environment. Still there are occasions when they must don a spacesuit designed mainly for environmental control and mobility and leave the confines of their better-protected domain. This is especially true for deep space exploration. The impact of spacesuit construction on the exposure of critical astronaut organs will be examined in the ionizing radiation environments of free space, the lunar surface and the Martian surface. The computerized anatomical male model is used to evaluate astronaut self-shielding factors and to determine space radiation exposures to critical radiosensitive human organs.

Wilson, J. W.↗
NASA NTRS2008

Impaired Cytogenetic Damage Repair and Cell Cycle Regulation in Response to Ionizing Radiation in Human Fibroblast Cells with Individual Knock-down of 25 Genes

Changes of gene expression profile are one of the most important biological responses in living cells after ionizing radiation (IR) exposure. Although some studies have demonstrated that genes with upregulated expression induced by IR may play important roles in DNA damage sensing, cell cycle checkpoint and chromosomal repair, the relationship between the regulation of gene expression by IR and its impact on cytogenetic responses to ionizing radiation has not been systematically studied. In our present study, the expression of 25 genes selected based on their transcriptional changes in response to IR or from their known DNA repair roles were individually knocked down by siRNA transfection in human fibroblast cells. Chromosome aberrations (CA) and micronuclei (MN) formation were measured as the cytogenetic endpoints. Our results showed that the yield of MN and/or CA formation were significantly increased by suppressed expression of 5 genes that included Ku70 in the DSB repair pathway; XPA in the NER pathway; RPA1 in the MMR pathway; RAD17 and RBBP8 in cell cycle control. Knocked-down expression of 4 genes including MRE11A, RAD51 in the DSB pathway, and SESN1 and SUMO1 showed significant inhibition of cell cycle progression, possibly because of severe impairment of DNA damage repair. Furthermore, loss of XPA, p21 and MLH1 expression resulted in both enhanced cell cycle progression and significantly higher yield of cytogenetic damage, indicating the involvement of these gene products in both cell cycle control and DNA damage repair. Of these 11 genes that affected the cytogenetic response, 9 were up-regulated in the cells exposed to gamma radiation, suggesting that genes transcriptionally modulated by IR were critical to regulating the biological consequences after IR. Failure to express these IR-responsive genes, such as by gene mutation, could seriously change the outcome of the post IR scenario and lead to carcinogenesis.

Zhang, Ye↗
NASA NTRS1975

Effects of ionizing radiation on charge-coupled imagers

The effects of ionizing radiation on three different charge coupled imagers have been investigated. Device performance was evaluated as a function of total gamma ray dose. The principal failure mechanisms have been identified for each particular device structure. The clock and bias voltages required for high total dose operation of the devices are presented.

Killiany, J. M.↗