Search NASA⌕ Search

SEARCH · Search NASA

Results for “RADIATION EXPOSURE”

Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9
All sourcesNASA NTRSDOE OSTI
NASA NTRS2007

The NASA-Sponsored Study of Cataract in Astronauts (NASCA). Relationship of Exposure to Radiation in Space and the Risk of Cataract Incidence and Progression. Report 1: Recruitment and Methodology

The NASA Study of Cataract in Astronauts (NASCA) is a five-year, multi-centered, investigation of lens opacification in populations of U.S. astronauts, military pilots, and ground-based (nonaviator) comparison participants. For astronauts, the explanatory variable of most interest is radiation exposure during space flight, however to properly evaluate its effect, the secondary effects of age, nutrition, general health, solar ocular exposure, and other confounding variables encountered in non-space flight must also be considered. NASCA contains an initial baseline, cross-sectional objective assessment of the severity of cortical (C), nuclear (N), and posterior subcapsular (PSC) lens opacification, and annual follow-on assessments of severity and progression of these opacities in the population of astronauts and in participants sampled from populations of military pilots and ground-based exposure controls. From these data, NASCA will estimate the degree to which space radiation affects lens opacification for astronauts and how the overall risks of each cataract type for astronauts compared with those of the other exposure control groups after adjusting for differences in age and other explanatory variables.

Chylack, Leo T.↗
NASA NTRS2011

Expression of Enzymes that Metabolize Medications

INTRODUCTION: Increased exposure to radiation is one physiological stressor associated with spaceflight and it is feasible to conduct ground experiments using known radiation exposures. The health of the liver, especially the activity rate of its metabolic enzymes, determines the concentration of circulating drugs as well as the duration of their efficacy. While radiation is known to alter normal physiological function, how radiation affects liver metabolism of administered medications is unclear. Crew health could be affected if the actions of medications used in spaceflight deviated from expectations formed during terrestrial medication use. This study is an effort to identify liver metabolic enzymes whose expression is altered by spaceflight or by radiation exposures that mimic features of the spaceflight environment. METHODS: Using procedures approved by the Animal Care and Use Committee, mice were exposed to either 137Cs (controls, 50 mGy, 6Gy, or 50 mGy + 6Gy separated by 24 hours) or 13 days of spaceflight on STS 135. Animals were anesthetized and sacrificed at several time points (4 hours, 24 hours or 7 days) after their last radiation exposure, or within 6 hours of return to Earth for the STS 135 animals. Livers were removed immediately and flash-frozen in liquid nitrogen. Tissue was homogenized, RNA extracted, purified and quality-tested. Complementary DNA was prepared from high-quality RNA samples, and used in RT-qPCR experiments to determine relative expression of a wide variety of genes involved in general metabolism and drug metabolism. RESULTS: Results of the ground radiation exposure experiments indicated ~65 genes of the 190 tested were significantly affected by at least one of the radiation doses. Many of the affected genes are involved in the metabolism of drugs with hydrophobic or steroid-like structures, maintenance of redox homeostasis and repair of DNA damage. Most affected genes returned to near control expression levels by 7 days post-treatment. Not all recovered completely by the final time point tested: with 6 Gy exposure, metallothionein expression was 132-fold more than control at the 4 hr time point, and fell at each later time point (11-fold at 24 hrs, and 8-fold at 7 days). In contrast, there were other genes whose expression was altered and remained relatively constant through the 7 day period we tested. One examples is Cyp17a1, which showed a 4-fold elevation at 4 hrs after exposure and remained constant for 7 days after the last treatment. Spaceflight samples evaluated with similar methods and comparisons will be made between the radiation-treated groups and the spaceflight samples. CONCLUSION It seems likely that radiation exposure triggers homeostatic mechanisms, which could include alterations of gene expression. Better understanding of these pathways could aid in optimizing medications doses given to crewmembers who require treatment and eventually, to development of new countermeasures to ameliorate or prevent radiation-induced damage to cells and tissues.

Wotring, V. E.↗
NASA NTRS2011

Radio-Adaptive Responses of Mouse Myocardiocytes

One of the most significant occupational hazards to an astronaut is the frequent exposure to radiation. Commonly associated with increased risk for cancer related morbidity and mortality, radiation is also known to increase the risk for cardiovascular related disorders including: pericarditis, hypertension, and heart failure. It is believed that these radiation-induced disorders are a result of abnormal tissue remodeling. It is unknown whether radiation exposure promotes remodeling through fibrotic changes alone or in combination with programmed cell death. Furthermore, it is not known whether it is possible to mitigate the hazardous effects of radiation exposure. As such, we assessed the expression and mechanisms of radiation-induced tissue remodeling and potential radio-adaptive responses of p53-mediated apoptosis and fibrosis pathways along with markers for oxidative stress and inflammation in mice myocardium. 7 week old, male, C57Bl/6 mice were exposed to 6Gy (H) or 5cGy followed 24hr later with 6Gy (LH) Cs-137 gamma radiation. Mice were sacrificed and their hearts extirpated 4, 24, or 72hr after final irradiation. Real Time - Polymerase Chain Reaction was used to evaluate target genes. Pro-apoptotic genes Bad and Bax, pro-cell survival genes Bcl2 and Bcl2l2, fibrosis gene Vegfa, and oxidative stress genes Sod2 and GPx4 showed a reduced fold regulation change (Bad,-6.18; Bax,-6.94; Bcl2,-5.09; Bcl2l2,-4.03; Vegfa, -11.84; Sod2,-5.97; GPx4*,-28.72; * = Bonferroni adjusted p-value . 0.003) 4hr after H, but not after 4hr LH when compared to control. Other p53-mediated apoptosis genes Casp3, Casp9, Trp53, and Myc exhibited down-regulation but did not achieve a notable level of significance 4hr after H. 24hr after H, genetic down-regulation was no longer present compared to 24hr control. These data suggest a general reduction in genetic expression 4hrs after a high dose of gamma radiation. However, pre-exposure to 5cGy gamma radiation appears to facilitate a radio-adaptive response that mitigates the reduction in genetic expression associated with single high-dose gamma radiation exposure. This radio-adaptive response may serve as a potential countermeasure to radiation-induced myocardial remodeling and preserve the cardiovascular health of astronauts; thus, reducing the risks of human space exploration.

Seawright, John W.↗
NASA NTRS2011

Induction of a Radio-Adaptive Response by Low-dose Gamma Irradiation in Mouse Cardiomyocytes

One of the most significant occupational hazards to an astronaut is the frequent exposure to radiation. Commonly associated with increased risk for cancer related morbidity and mortality, radiation is also known to increase the risk for cardiovascular related disorders including: pericarditis, hypertension, and heart failure. It is believed that these radiation-induced disorders are a result of abnormal tissue remodeling. It is unknown whether radiation exposure promotes remodeling through fibrotic changes alone or in combination with programmed cell death. Furthermore, it is not known whether it is possible to mitigate the hazardous effects of radiation exposure. As such, we assessed the expression and mechanisms of radiation-induced tissue remodeling and potential radio-adaptive responses of p53-mediated apoptosis and fibrosis pathways along with markers for oxidative stress and inflammation in mice myocardium. 7 week old, male, C57Bl/6 mice were exposed to 6Gy (H) or 5cGy followed 24hr later with 6Gy (LH) 137Cs gamma radiation. Mice were sacrificed and their hearts extirpated 4, 24, or 72hr after final irradiation. Real Time - Polymerase Chain Reaction was used to evaluate target genes. Apoptotic genes Bad and Bax, pro-cell survival genes Bcl2 and Bcl2l2, fibrosis gene Vegfa, and oxidative stress genes Sod2 and GPx4 showed a reduced fold regulation change (Bad,-6.18; Bax,-6.94; Bcl2,-5.09; Bcl2l2,-4.03; Vegfa, -11.84; Sod2,-5.97; GPx4*,-28.72; * = Bonferroni adjusted p-value < or = 0.003) 4hr after H, but not after 4hr LH compared to control. Other p53-mediated apoptosis genes Casp3, Casp9, Trp53, and Myc exhibited down-regulation but did not achieve a notable level of significance 4hr after H. 24hr after H, genetic down-regulation was no longer present compared to 24hr control. These data suggest a general reduction in genetic expression 4hrs after a high dose of gamma radiation. However, pre-exposure to 5cGy gamma radiation appears to facilitate a radio-adaptive response that mitigates the reduction in genetic expression associated with single high-dose gamma radiation exposure. This radio-adaptive response may serve as a potential countermeasure to radiation-induced myocardial remodeling and preserve the cardiovascular health of astronauts; thus, reducing the risks of human space exploration.

Westby, Christian M.↗
NASA NTRS2003

Is there a common mechanism underlying genomic instability, bystander effects and other nontargeted effects of exposure to ionizing radiation?

A number of nontargeted and delayed effects associated with radiation exposure have now been described. These include radiation-induced genomic instability, death-inducing and bystander effects, clastogenic factors and transgenerational effects. It is unlikely that these nontargeted effects are directly induced by cellular irradiation. Instead, it is proposed that some as yet to be identified secreted factor can be produced by irradiated cells that can stimulate effects in nonirradiated cells (death-inducing and bystander effects, clastogenic factors) and perpetuate genomic instability in the clonally expanded progeny of an irradiated cell. The proposed factor must be soluble and capable of being transported between cells by cell-to-cell gap junction communication channels. Furthermore, it must have the potential to stimulate cellular cytokines and/or reactive oxygen species. While it is difficult to imagine a role for such a secreted factor in contributing to transgenerational effects, the other nontargeted effects of radiation may all share a common mechanism.

Non-NASA Center↗
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 NTRS2009

Analytic Shielding Optimization to Reduce Crew Exposure to Ionizing Radiation Inside Space Vehicles

A sustainable lunar architecture provides capabilities for leveraging out-of-service components for alternate uses. Discarded architecture elements may be used to provide ionizing radiation shielding to the crew habitat in case of a Solar Particle Event. The specific location relative to the vehicle where the additional shielding mass is placed, as corroborated with particularities of the vehicle design, has a large influence on protection gain. This effect is caused by the exponential- like decrease of radiation exposure with shielding mass thickness, which in turn determines that the most benefit from a given amount of shielding mass is obtained by placing it so that it preferentially augments protection in under-shielded areas of the vehicle exposed to the radiation environment. A novel analytic technique to derive an optimal shielding configuration was developed by Lockheed Martin during Design Analysis Cycle 3 (DAC-3) of the Orion Crew Exploration Vehicle (CEV). [1] Based on a detailed Computer Aided Design (CAD) model of the vehicle including a specific crew positioning scenario, a set of under-shielded vehicle regions can be identified as candidates for placement of additional shielding. Analytic tools are available to allow capturing an idealized supplemental shielding distribution in the CAD environment, which in turn is used as a reference for deriving a realistic shielding configuration from available vehicle components. While the analysis referenced in this communication applies particularly to the Orion vehicle, the general method can be applied to a large range of space exploration vehicles, including but not limited to lunar and Mars architecture components. In addition, the method can be immediately applied for optimization of radiation shielding provided to sensitive electronic components.

Gaza, Razvan↗
NASA NTRS2009

Overview of Materials International Space Station Experiment 7B

Materials International Space Station Experiment 7B (MISSE 7B) is the most recent in a series of experiments flown on the exterior of International Space Station for the purpose of determining the durability of materials and components in the space environment. A collaborative effort among the Department of Defense, the National Aeronautics and Space Administration, industry, and academia, MISSE 7B will be flying a number of NASA experiments designed to gain knowledge in the area of space environmental effects to mitigate risk for exploration missions. Consisting of trays called Passive Experiment Containers, the suitcase sized payload opens on hinges and allows active and passive experiments contained within to be exposed to the ram and wake or zenith and nadir directions in low Earth orbit, in essence, providing a test bed for atomic oxygen exposure, ultraviolet radiation exposure, charged particle radiation exposure, and thermal cycling. New for MISSE 7B is the ability to monitor experiments actively, with data sent back to Earth via International Space Station communications. NASA?s active and passive experiments cover a range of interest for the Agency. Materials relevant to the Constellation Program include: solar array materials, seal materials, and thermal protection system materials. Materials relevant to the Exploration Technology Development Program include: fabrics for spacesuits, materials for lunar dust mitigation, and new thermal control coatings. Sensors and components on MISSE 7B include: atomic oxygen fluence monitors, ultraviolet radiation sensors, and electro-optical components. In addition, fundamental space environmental durability science experiments are being flown to gather atomic oxygen erosion data and thin film polymer mechanical and optical property data relevant to lunar lander insulation and the James Web Space Telescope. This paper will present an overview of the NASA experiments to be flown on MISSE 7B, along with a summary of the thermal environment to be expected during the 1 yr mission scheduled for launch in 2009.

Jaworske, Donald A.↗