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Results for “Oxidative damage”

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.

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At least 55 records · Page 3
All sourcesNASA NTRSDOE OSTI
NASA NTRS2000

Cell signaling by reactive nitrogen and oxygen species in atherosclerosis

The production of reactive oxygen and nitrogen species has been implicated in atherosclerosis principally as means of damaging low-density lipoprotein that in turn initiates the accumulation of cholesterol in macrophages. The diversity of novel oxidative modifications to lipids and proteins recently identified in atherosclerotic lesions has revealed surprising complexity in the mechanisms of oxidative damage and their potential role in atherosclerosis. Oxidative or nitrosative stress does not completely consume intracellular antioxidants leading to cell death as previously thought. Rather, oxidative and nitrosative stress have a more subtle impact on the atherogenic process by modulating intracellular signaling pathways in vascular tissues to affect inflammatory cell adhesion, migration, proliferation, and differentiation. Furthermore, cellular responses can affect the production of nitric oxide, which in turn can strongly influence the nature of oxidative modifications occurring in atherosclerosis. The dynamic interactions between endogenous low concentrations of oxidants or reactive nitrogen species with intracellular signaling pathways may have a general role in processes affecting wound healing to apoptosis, which can provide novel insights into the pathogenesis of atherosclerosis.

Review, Tutorial↗
NASA NTRS1986

Effect of hard particle impacts on the atomic oxygen survivability of reflector surfaces with transparent protective overcoats

Silver mirror samples with protective coatings were subjected to a stream of 27 microns alumina particles to induce pinhole defects. The protective coating consisted of a layer of aluminum dioxide over silver followed by a layer of silicon dioxide over the alumina. Samples were prepared on both graphite-epoxy composite and fused quartz substrates. After exposure to the hard particle stream, the samples were exposed to an oxygen plasma environment in a laboratory plasma asher. The effects of both the hard particles and the oxygen plasma were documented by both reflectance measurements and scanning electron microscopy. The results indicated that oxidative damage to the silver reflecting layer continues beyond that of the erosively exposed silver. Oxidative undercutting of the silver layer and graphite-epoxy substrate continues in undamaged areas through adjacent, particle damaged defect sites. This may have implications for the use of such mirrors in a space station solar dynamic power system.

Gulino, D. A.↗
NASA NTRS1987

Effect of hard particle impacts on the atomic oxygen survivability of reflector surfaces with transparent protective overcoats

Silver mirror samples with protective coatings were subjected to a stream of 27 microns alumina particles to induce pinhole defects. The protective coating consisted of a layer of aluminum dioxide over silver followed by a layer of silicon dioxide over the alumina. Samples were prepared on both graphite-epoxy composite and fused quartz substrates. After exposure to the hard particle stream, the samples were exposed to an oxygen plasma environment in a laboratory plasma asher. The effects of both the hard particles and the oxygen plasma were documented by both reflectance measurements and scanning electron microscopy. The results indicated that oxidative damage to the silver reflecting layer continues beyond that of the erosively exposed silver. Oxidative undercutting of the silver layer and graphite-epoxy substrate continues in undamaged areas through adjacent, particle damaged defect sites. This may have implications for the use of such mirrors in a space station solar dynamic power system.

Gulino, Daniel A.↗
NASA NTRS2015

Induction of Oxidation in Living Cells by Time-Varying Electromagnetic Fields

We are studying how biological systems can harness quantum effects of time varying electromagnetic (EM) waves as the time-setting basis for universal biochemical organization via the redox cycle. The effects of extremely weak EM field on the biochemical redox cycle can be monitored through real-time detection of oxidation-induced light emissions of reporter molecules in living cells. It has been shown that EM fields can also induce changes in fluid transport rates through capillaries (approximately 300 microns inner diameter) by generating annular proton gradients. This effect may be relevant to understanding cardiovascular dis-function in spaceflight, beyond the ionosphere. Importantly, we show that these EM effects can be attenuated using an active EM field cancellation device. Central for NASA's Human Research Program is the fact that the absence of ambient EM field in spaceflight can also have a detrimental influence, namely via increased oxidative damage, on DNA replication, which controls heredity.

oxidation↗
NASA NTRS2007

Stochastic Effects in Computational Biology of Space Radiation Cancer Risk

Estimating risk from space radiation poses important questions on the radiobiology of protons and heavy ions. We are considering systems biology models to study radiation induced repair foci (RIRF) at low doses, in which less than one-track on average transverses the cell, and the subsequent DNA damage processing and signal transduction events. Computational approaches for describing protein regulatory networks coupled to DNA and oxidative damage sites include systems of differential equations, stochastic equations, and Monte-Carlo simulations. We review recent developments in the mathematical description of protein regulatory networks and possible approaches to radiation effects simulation. These include robustness, which states that regulatory networks maintain their functions against external and internal perturbations due to compensating properties of redundancy and molecular feedback controls, and modularity, which leads to general theorems for considering molecules that interact through a regulatory mechanism without exchange of matter leading to a block diagonal reduction of the connecting pathways. Identifying rate-limiting steps, robustness, and modularity in pathways perturbed by radiation damage are shown to be valid techniques for reducing large molecular systems to realistic computer simulations. Other techniques studied are the use of steady-state analysis, and the introduction of composite molecules or rate-constants to represent small collections of reactants. Applications of these techniques to describe spatial and temporal distributions of RIRF and cell populations following low dose irradiation are described.

Cucinotta, Francis A.↗
NASA NTRS2006

The Role of Non-Targeted Effects as Mediators in the Biological Effects of Proton Irradiation

In recent years, the hypothesis that non-DNA targets are primary initiators and mediators of the biological effects of ionizing radiation, such as proton beams and heavy ions, has gained much interest. These phenomena have been denoted as non-targeted or bystander effects to distinguish them from the more traditionally studied model that focuses on direct damage to DNA causing chromosomal rearrangements and mutations as causative of most biological endpoints such as cell killing, tissue damage, and cancer. We review cellular and extra-cellular structures and signal transduction pathways that have been implemented in these recent studies. Non-targeted effects of interest include oxidative damage to the cytoplasm and mitochondria, disruption of the extra-cellular matrix, and modification of cytokine signaling including TGF-beta, and gap junction communication. We present an introduction to these targets and pathways, and contrast there role with DNA damage pathways.

Cucinotta, Francis A.↗
NASA NTRS2017

Skeletal Responses to Long-Duration Simulated Weightlessness in Rats

Damaging effects due to spaceflight and long-duration weightlessness are seen in the musculoskeletal system, specifically with regards to bone loss, bone resorption, and changes in overall bone structure. These adverse effects are all seen with indicators of oxidative stress and a variation in the levels of oxidative gene expression. Once gravity is restored, however, the recovery is slow and incomplete. Despite this, few reports have investigated the correlation between oxidative damage and general modifications within the bone. In this project, we will make use of a ground-based model of simulated weightlessness (hindlimb unloading, HU) in order to observe skeletal changes in response to induced microgravity due to changes in oxidative pressures. With this model we will analyze samples at 14-day and 90-day time points following HU for the determination of acute and chronic effects, each with corresponding controls. We hypothesize that simulated microgravity will lead to skeletal adaptations including time-dependent activation of pro-oxidative processes and pro-osteoclastogenic signals related to the progression, plateau, and recovery of the bone. Microcomputed tomography techniques will be utilized to measure skeletal changes in response to HU. With the results of this study, we hope to further the understanding of skeletal affects as a result of long-duration weightlessness and develop countermeasures to combat bone loss in spaceflight and osteoporosis on Earth.

hindlimb unloading↗
NASA NTRS2002

Space flight and oxidative stress

Space flight is associated with an increase in oxidative stress after return to 1g. The effect is more pronounced after long-duration space flight. The effects lasts for several weeks after landing. In humans there is increased lipid peroxidation in erythrocyte membranes, reduction in some blood antioxidants, and increased urinary excretion of 8-iso-prostaglandin F(2alpha) and 8-oxo-7,8 dihydro-2 deoxyguanosine. Isoprostane 8-iso-prostaglandin F(2alpha) and 8-oxo-7,8 dihydro-2 deoxyguanosine are markers for oxidative damage to lipids and DNA, respectively. The changes have been attributed to a combination of the energy deficiency that occurs during flight and substrate competition for amino acids occurring between repleting muscle and other tissues during the recovery phase. The observations in humans have been complemented by rodent studies. Most rodent studies showed increased production of lipid peroxidation products postflight and decreased antioxidant enzyme activity postflight. The rodent observations were attributed to the stress associated with reentry into Earth's gravity. Decreasing the imbalance between the production of endogenous oxidant defenses and oxidant production by increasing the supply of dietary antioxidants may lessen the severity of the postflight increase in oxidative stress.

long duration↗
NASA NTRS1982

Influence of deformation behavior, oxydation, and temperature on the long time cyclic stress behavior of high temperature steels

The influence of different parameters on the creep-fatigue behavior of several steel alloys was investigated. The higher the temperature the lower the crack initiation value. Pauses during the cycle reduce the damage. Oxidation reduces and protective gas increases the lifetime. Prior loading and prior deformation reduce the lifetime. Short annealing slightly affects the cycle stress behavior. The test results do not satisfactorily agree with methods of extrapolation and damage accumulation.

Maile, K.↗
NASA NTRS1985

Thermal barrier coating life prediction model development

A methodology was established to predict thermal barrier coating life in an environment simulative of that experienced by gas turbine airfoils. Specifically, work is being conducted to determine failure modes of thermal barrier coatings in the aircraft engine environment. Analytical studies coupled with appropriate physical and mechanical property determinations are being employed to derive coating life prediction model(s) on the important failure mode(s). An initial review of experimental and flight service components indicates that the predominant mode of TBC failure involves thermomechanical spallation of the ceramic coating layer. This ceramic spallation involves the formation of a dominant crack in the ceramic coating parallel to and closely adjacent to the metal-ceramic interface. Initial results from a laboratory test program designed to study the influence of various driving forces such as temperature, thermal cycle frequency, environment, and coating thickness, on ceramic coating spalling life suggest that bond coat oxidation damage at the metal-ceramic interface contributes significantly to thermomechanical cracking in the ceramic layer. Low cycle rate furnace testing in air and in argon clearly shows a dramatic increase of spalling life in the non-oxidizing environments.

Sheffler, K. D.↗
NASA NTRS2014

Chronic Lunar Dust Exposure on Rat Cornea: Evaluation by Gene Expression Profiling

Lunar dust is capable of entering habitats and vehicle compartments by sticking to spacesuits or other objects that are transferred into the spacecraft from the lunar surface and has been reported to cause irritation upon exposure. During the Apollo missions, crewmembers reported irritation specifically to the skin and eyes after contamination of the lunar and service modules. It has since been hypothesized that ocular irritation and abrasion might occur as a result of such exposure, impairing crew vision. Recent work has shown that both ultrafine and unground lunar dust exhibited minimal irritancy of the ocular surface (i.e., cornea); however, the assessment of the severity of ocular damage resulting from contact of lunar dust particles to the cornea has focused only on macroscopic signs of mechanical irritancy and cytotoxicity. Given the chemical reactive properties of lunar dust, exposure of the cornea may contribute to detrimental effects at the molecular level including but not limited to oxidative damage. Additionally, low level chronic exposures may confound any results obtained in previous acute studies. We report here preliminary results from a tissue sharing effort using 10‐week‐old Fischer 344 male rats chronically exposed to filtered air or jet milled lunar dust collected during Apollo 14 using a Jaeger‐NYU nose‐only chamber for a total of 120 hours (6 hours daily, 5 days a week) over a 4‐week period. RNA was isolated from corneas collected from rats at 1 day and 7 days after being exposed to concentrations of 0, 20, and 60 mg/m3 of lunar dust. Microarray analysis was performed using the Affymetrix GeneChip Rat Genome 230 2.0 Array with Affymetrix Expression Console and Transcriptome Analysis Console used for normalization and secondary analysis. An Ingenuity iReport"TM" was then generated for canonical pathway identification. The number of differentially expressed genes identified increases with dose compared to controls suggesting a more severe response to the lunar dust insult at higher levels. Pathways of interests that have been identified in all exposed samples include oxidative stress response, mitochondrial dysfunction, fibrosis, epithelial healing, TGF-Beta signaling, and extracellular matrix remodeling. Several biological processes related to cell migration, cellular proliferation, and eye development were also identified to be altered by exposure to lunar dust. Our preliminary results suggest that even a chronic insult of lunar dust as low as 20 mg/m(exp 3) elicits a molecular response in cornea tissue. Lunar dust on the surface of the moon would have the added properties of ionization and activation potentially leading to further damage to the cornea and greater sensitivity to any other environmental insult such as exposure to radiation. Additional studies are required to fully assess the risk of vision impairment and the mechanistic responses initiated in cornea exposed to lunar dust as well as the potential for long‐term effects to astronaut health

Theriot, C. A.↗
NASA NTRS2012

Spaceflight Effects and Molecular Responses in the Mouse Eye: Observations after NASA Shuttle Mission STS-133

Background: Human space exploration implies a combination of stressors including microgravityinduced cephalad fluid shift and radiation exposure. Ocular changes in astronauts leading to visual impairment are of occupational health relevance. The effect of this complex environment on ocular morphology and function is poorly understood. Material and Methods: Mice were assigned to a Flight (FLT) group flown on shuttle mission STS133, Animal Enclosure Module (AEM), or vivarium (VIV) ground controls. Eyes were collected at 1, 5 and 7 days after landing, and were fixed for histological sectioning. The contralateral eye was used for gene expression profiling by qRT-PCR. Routine histology and immunohistochemistry using 8-hydroxy-2'-deoxyguanosine (8-OHdG), caspase-3, glial fibrillary acidic protein (GFAP) and beta-amyloid were used to study the eyes. Results and Conclusions: 8-OHdG and caspase-3 immunoreactivity was increased in the retina in FLT samples at return from flight (R+1) compared to ground controls, and decreased at day 7 (R+7), suggesting an increase in oxidative stress and cell apoptosis. FLT mice showed evidence of retinal pigment epithelium (RPE) apoptosis possibly secondary to oxidative damage. Although attenuation of RPE has been related to retinal choroidal folds in astronauts, it is yet to be determined whether or not increased RPE apoptosis may contribute to the formation of choroidal folds or may increase the risk for other retinal pathologies, such as AMD. beta-amyloid was seen in the nerve fibers at the post-laminar region of the optic nerve in the flight samples (R+7). Deposition of beta-amyloid has a strong correlation with mechanical trauma. The coexpression of GFAP in astrocytes and oligodentrocytes in these same areas supports the possible mechanical origin probably secondary to intracranial pressure that is transmitted into the nerve, as a result of an increase in venous pressure associated to microgravity-induced cephalic fluid shift. However, there is the need to further investigate the nature of the changes through additional experimental work. Gene expression of oxidative and cellular stress response genes was unregulated in the retina of FLT samples upon landing followed by lower levels by R+7. These results suggest that reversible molecular damage occurs in the retina of mice exposed to spaceflight and that protective cellular and molecular pathways are induced in the retina in response to these changes.

ProsperoPonce, Claudia Maria↗
NASA NTRS2024

Metabolic Stress in Space: ROS-Induced Mutations in Mice Hint at A New Path to Cancer

Long-duration spaceflight beyond Earth's magnetosphere poses serious health risks, including muscle atrophy, bone loss, liver and kidney damage, and the Spaceflight-Associated Neuro-ocular Syndrome (SANS). RNA-seq of mice aboard the International Space Station (ISS) for 37 days revealed extraordinary hypermutation in tissue-specific genes, with guanine base conversion predominating, potentially contributing to spaceflight-associated health risks. Our results suggest that the genome-wide accelerated mutation that we measured, seemingly independent of radiation dose, was induced by oxidative damage from higher atmospheric carbon dioxide (CO 2 ) levels and increased reactive oxygen species (ROS) on the ISS. This accelerated mutation, faster via RNA transcription than replication and more numerous than by radiation alone, unveils novel hotspots in the mammalian proteome. Notably, these hotspots correlate with commonly mutated genes across various human cancers, highlighting the ISS as a crucial platform for studying accelerated mutation, genome instability, and the induction of disease-causing mutations in model organisms. Our results suggest that metabolic processes can contribute to somatic mutation, and thus may play a role in the development of cancer. A metabolic link to genetic instability potentially has far-reaching implications for various diseases, with implications for human health on Earth and in space.

mice↗
NASA NTRS2020

High productivity in hybrid-poplar plantations without isoprene emission to the atmosphere

Hybrid-poplar tree plantations provide a source for biofuel and biomass, but they also increase forest isoprene emissions. The consequences of increased isoprene emissions include higher rates of tropospheric ozone production, increases in the lifetime of methane, and increases in atmospheric aerosol production, all of which affect the global energy budget and/or lead to the degradation of air quality. Using RNA interference (RNAi) to suppress isoprene emission, we show that this trait, which is thought to be required for the tolerance of abiotic stress, is not required for high rates of photosynthesis and woody biomass production in the agroforest plantation environment, even in areas with high levels of climatic stress. Biomass production over 4 y in plantations in Arizona and Oregon was similar among genetic lines that emitted or did not emit significant amounts of isoprene. Lines that had substantially reduced isoprene emission rates also showed decreases in flavonol pigments, which reduce oxidative damage during extremes of abiotic stress, a pattern that would be expected to amplify metabolic dysfunction in the absence of isoprene production in stress-prone climate regimes. However, compensatory increases in the expression of other proteomic components, especially those associated with the production of protective compounds, such as carotenoids and terpenoids, and the fact that most biomass is produced prior to the hottest and driest part of the growing season explain the observed pattern of high biomass production with low isoprene emission. Our results show that it is possible to reduce the deleterious influences of isoprene on the atmosphere, while sustaining woody biomass production in temperate agroforest plantations.

oxidative stress↗
NASA NTRS2018

Prevention of Spaceflight-Induced Bone Loss: A Promising Dietary Countermeasure

Space radiation is one of the challenges for long-term spaceflight, especially for missions beyond low Earth Orbit. We have shown that a diet composed of 25% dried plum (DP) prevents radiation-induced bone loss. The DP diet fully protected the cancellous bone microarchitecture of mice exposed to ionizing radiation (gamma, proton, and HZE). In particular relevant to space radiation, we showed that the DP diet prevents bone loss due to 1Gy of sequential exposure of proton (1H, low linear energy transfer -LET-), and 1Gy of iron (56Fe, high-LET). In addition, total body exposure to 1Gy of HZE radiation (56Fe) impaired the osteoprogenitors in mice fed the control diet, as indicated by decreased osteoblast mineralization. In contrast, marrow stem cells from mice fed the DP did not exhibit these deficits. Based on these promising results supporting DP as a countermeasure to prevent space radiation induced-tissue damage, we conducted additional studies to combine radiation and simulated microgravity. We exposed skeletally mature male mice to simulated microgravity (using hindlimb unloading, HU) or total body irradiation (TBI, 2Gy 137Cs) or in combination (HU+TBI). We observed bone loss in the mice fed the control diet (CD) exposed to simulated spaceflight, as measured by cancellous bone microarchitecture parameters such as percent bone volume (BV/TV). In contrast, mice fed the DP diet did not exhibit similar bone loss with either treatments (HU or TBI) or combined (HU+TBI) as seen in most parameters. This was observed in both long bones (tibia) and axial bones (vertebrae). Furthermore, preliminary data shows that pre-feeding with the DP diet attenuates the HU-induced decrement in bone-forming osteoblasts colony counts and mineralization capacity of the osteoprogenitor cells. We also performed DP feeding at lower doses (5%, 10%) and found that these doses are less effective in preventing the radiation-induced bone loss. All our studies with the DP diet as a countermeasure were done with a period of pre-feeding ranging from 14 to 21 days before irradiation, and in order to test the capacity of the DP diet as a countermeasure provided after exposure to radiation, we exposed mice to 2Gy gamma radiation and then provided the DP diet 24 hours post-IR. Preliminary data indicates that DP mitigated the radiation-induced deficits in certain cancellous bone structural parameters. Finally, we showed that mice fed with the control diet (CD) increased oxidative damage in the serum after radiation exposure, whereas mice fed the DP diet do did not show such an increase. In summary, the DP diet is a promising countermeasure for spaceflight-induced tissue damage.

Schreurs, Ann-Sofie↗
NASA NTRS1986

Application of photosynthetic N2-fixing cyanobacteria to the CELSS program

Commercially available air lift fermentors were used to simultaneously monitor biomass production, N2-fixation, photosynthesis, respiration, and sensitivity to oxidative damage during growth under various nutritional and light regimes, to establish a data base for the integration of these organisms into a Closed Ecological Life Support System (CELSS) program. Certain cyanobacterial species have the unique ability to reduce atmospheric N2 to organic nitrogen. These organisms combine the ease of cultivation characteristics of prokaryotes with the fully developed photosynthetic apparatus of higher plants. This, along with their ability to adapt to changes in their environment by modulation of certain biochemical pathways, make them attractive candidates for incorporation into the CELSS program.

Packer, L.↗
NASA NTRS1986

Effects of temperature and hold times on low cycle fatigue of Astroloy

Low cycle fatigue (LCF) and creep-fatigue-environment interactions of HIP Astroloy were studied at 650 C and 725 C. The results showed that the model proposed by Kaisand and Mowbray (1979) was successful in predicting the magnitude and trend of the fatigue crack growth rate from LCF data. Raising the temperature from 650 C to 725 C did not change the fracture mode, while employing tensile hold caused a change in fracture mode and was more damaging than raising the temperature by 75 C. All samples displayed multiple fracture origins, which is initiated transgranularly in continuous cycling tests and intergranularly in hold time tests. An examination of the secondary crack showed no apparent creep damage. Oxidation in high purity argon appeared to be the major factor in LCF life degradation due to hold time.

Choe, S. J.↗