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122 results for “reactive oxygen species”
Hybrid lizards with introgressed mtDNA show increased resistance to DNA damage from Reactive Oxygen Species
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Fifteen physiological traits related to osmoregulation and reactive oxygen species metabolism in two life form aquatic plants under a natural water salinity gradient on the Tibetan Plateau and Northwest China
<p><span>Aquatic plants, as the primary producers, determine the community structure and ecological function of freshwater ecosystems. However, salinization threatens inland freshwater wetlands and thus the survival of aquatic plants. Exploring the plant physiological responses to increasing water salinity could enhance our understandings of plant adaptive strategies under future climate change regimes in wetlands. We measured 15 physiological traits of 49 aquatic plant species along a large environmental gradient in alpine and arid regions of western China, to explore the physiological adaptions and compare the similarities and differences in adaptive strategies between the two life forms to natural water salinity. We found that both water salinity and low temperature were key factors affecting aquatic plants in alpine and arid regions. Aquatic plants adapt to saline habitats by accumulating proline and sulfur (S) concentrations, and to cold habitats by increasing ascorbate peroxidase activity. Plant trait network analysis showed that the hub trait in emergent plants was S, but in submerged plants was proline, suggesting that emergent plants balanced osmoregulation and reactive oxygen metabolism via S-containing compounds, while submerged plants prioritizing the regulation of osmotic balance via proline.</span></p>
Predominance of Secondary Organic Aerosol to Particle-bound Reactive Oxygen Species Activity in Fine Ambient Aerosol
<p>Reactive oxygen species (ROS) are believed to contribute to the adverse health effects of aerosols. This may happen by inhaled particle-bound (exogenic) ROS (PB-ROS) or by ROS formed within the respiratory tract by certain aerosol components (endogenic ROS). We investigated the chemical composition of aerosols and their exogenic ROS content at the two contrasting locations Beijing (China) and Bern (Switzerland). We apportioned the ambient organic aerosol to different sources and attributed the observed water-soluble PB-ROS to them. The oxygenated organic aerosol (OOA, a proxy for secondary organic aerosol, SOA) explained the highest fraction of the exogenic ROS concentration variance at both locations. We also characterized primary and secondary aerosol emissions generated from different biogenic and anthropogenic sources in smog chamber experiments. The exogenic PB-ROS content in the OOA from these emission sources was comparable to that in the ambient measurements. Our results imply that SOA from gaseous precursors of different anthropogenic emission sources is a crucial source of water-soluble PB-ROS and should be additionally considered in toxicological and epidemiological studies in an adequate way besides primary emissions. The importance of PB-ROS may be connected to the seasonal trends in health effects of PM reported by epidemiological studies, with elevated incidences of adverse effects in warmer seasons, which are accompanied by more intense atmospheric oxidation processes.</p>
Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production
<p>Dataset associated with publication "Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production"</p>
Fifteen physiological traits related to osmoregulation and reactive oxygen species metabolism in two life form aquatic plants under a natural water salinity gradient on the Tibetan Plateau and Northwest China
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Data for: Mitochondrial Ca2+-coupled generation of reactive oxygen species, peroxynitrite formation, and endothelial dysfunction in Cantú syndrome
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Lemon zinc finger protein ClSUP induces the accumulation of reactive oxygen species and inhibits citrus yellow vein-clearing virus infection via interactions with ClDOF3.4
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Parvalbumin expression in oligodendrocyte-like CG4 cells causes a reduction in mitochondrial volume, attenuation in reactive oxygen species production and a decrease in cell processes' length and branching
<p>Forebrain glial cells - ependymal cells and astrocytes -acquire upon injury- a “reactive” phenotype associated with parvalbumin (PV) upregulation. Since free radicals, e.g. reactive oxygen species (ROS) play a role in the pathogenesis of multiple sclerosis, and that PV-upregulation in glial cells is inversely correlated with the level of oxidative stress, we hypothesized that PV-upregulation might also protect oligodendrocytes by decreasing ROS production. Lentiviral transduction techniques allowed for PV overexpression in CG4 oligodendrocyte progenitor cells (OPCs). Depending on the growth medium CG4 cells can be maintained in an OPC-like state, or induced to differentiate into an oligodendrocyte (OLG)-like phenotype. While increased levels of PV had no effect on cell proliferation and invasiveness <em>in vitro</em>, PV decreased the mitochondria volume in CG4 cell bodies, as well as the mitochondrial density in CG4 processes in both OPC-like and OLG-like states. In line with the PV-induced global decrease in mitochondrial volume, elevated PV levels reduced transcript levels of mitochondrial transcription factors involved in mitochondria biogenesis. In differentiated PV-overexpressing CG4 cells with a decreased mitochondrial volume, UV-induced ROS production was lower than in control CG4 cells hinting towards a possible role of PV in counteracting oxidative stress. Unexpectedly, PV also decreased the length of processes in undifferentiated CG4 cells and moreover diminished branching of differentiated CG4 cell processes, strongly correlated with the decreased density of mitochondria in CG4 cell processes. Thus besides conferring a protective role against oxidative stress, PV in a cell autonomous fashion additionally affects process’ growth and branching in CG4 cells.</p>
Fig. 1 in Reactive oxygen species in cell wall metabolism and development in plants
Fig. 1. Schematic representation of the enzymes at the plasma membrane and in the cell wall that are able to form reactive oxygen species (ROS: superoxide anion radical · — hydrogen peroxide hydroxyl radical. into the apoplast. · — is dismutated either enzymatically catalyzed by superoxide dismutase, (O 2 ), (H2O2), ( OH)) O 2 to H2O2 or nonenzymatically in the acidic pH that is typical in the cell wall. ROS play important roles both in cell wall loosening during cell elongation and cross-link formation involved in cell growth restriction..OH is considered as a cell wall-loosening agent formed from H O either non-enzymatically by Fenton reaction involving a transition metal such as 2 2 Fe2+ or Cu +, or enzymatically by peroxidases (not depicted). Di- and oligoferulate bridges, bonds between tyrosine residues abundant in cell wall structural proteins, lignin formation, or cross-linkages between ferulates and lignin are possible cross-links involved in cell growth restriction. For the cross-link formation, oxidative enzymes (peroxidase in a peroxidative cycle using H2O2 as an oxidant, or laccase using O2 as an oxidant) catalyze the oxidation of the phenolic residues after which they make a crosslink. In addition to cell wall modifications, ROS are important signalling components in various biological processes. The left cell shows the enzymes producing ROS, and the right cell shows the enzymes consuming ROS during cell wall cross-linking. Note that all enzymes and the cross-link types mentioned may not be present in the same cell, or in all species. In case of quinone reductases, further studies are needed to find out whether enough quinones are present in the plasma membranes to be able to mediate electron transport from the cytoplasmic reductant to apoplastic molecular oxygen.
Data from: Ligation of glycophorin A generates reactive oxygen species leading to decreased red blood cell function
Acute, inflammatory conditions associated with dysregulated complement activation are characterized by significant increases in blood concentration of reactive oxygen species (ROS) and ATP. The mechanisms by which these molecules arise are not fully understood. In this study, using luminometric- and fluorescence-based methods, we show that ligation of glycophorin A (GPA) on human red blood cells (RBCs) results in a 2.1-fold, NADPH-oxidase-dependent increase in intracellular ROS that, in turn, trigger multiple downstream cascades leading to caspase-3 activation, ATP release, and increased band 3 phosphorylation. Functionally, using 2D microchannels to assess membrane deformability, GPS-ligated RBCs travel 33% slower than control RBCs, and lipid mobility was hindered by 10% using fluorescence recovery after photobleaching (FRAP). These outcomes were preventable by pretreating RBCs with cell-permeable ROS scavenger glutathione monoethyl ester (GSH-ME). Our results obtained in vitro using anti-GPA antibodies were validated using complement-altered RBCs isolated from control and septic patients. Our results suggest that during inflammatory conditions, circulating RBCs significantly contribute to capillary flow dysfunctions, and constitute an important but overlooked source of intravascular ROS and ATP, both critical mediators responsible for endothelial cell activation, microcirculation impairment, platelet activation, as well as long-term dysregulated adaptive and innate immune responses.
Phototoxicity and Cell Passage Affect Intracellular Reactive Oxygen Species Levels and Sensitivity Towards Non-Thermal Plasma Treatment in Fluorescently-Labeled Cancer Cells
<p>Raw data for the manuscript "Phototoxicity and Cell Passage Affect Intracellular Reactive Oxygen Species Levels and Sensitivity Towards Non-Thermal Plasma Treatment in Fluorescently-Labeled Cancer Cells".</p>
Fig. 5 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 5. Nerolidol suppressed the protein and mRNA expression of ATM in rat leiomyoma cells. (A, B) ELT3 cells were treated with nerolidol for 48 h and were then harvested for the western blot analysis of phosphorylated ATM and total ATM (A) and for determining ATM mRNA expression using quantitative RT-PCR (B). GAPDH was used as the loading control. The inserted numbers in (A) represent the relative expression level compared to that of the vehicle control (indicated as 0 μM). (C, D, E, F) ELT3 cells were treated with the indicated concentrations of KU-55933, an ATM inhibitor, for 48 h, following which the cells were harvested for further analysis. (C) The expression levels of p-ATMser1981, total ATM, p-Aktser473, total Akt, CDK4, and CDK6 were determined using western blot analysis. β-Actin was used as the loading control. The inserted numbers in (C) represent the relative expression level compared to that of the vehicle control (indicated as 0 μM). (D, E) Cell cycle analysis was performed after propidium iodide staining and FACS, and the results were analyzed using the FlowJo software (D). The percentages of cells in each cell cycle phase are plotted in (E). (F) Cell proliferation was determined using the MTT assay. DMSO (0.1 %) was used as the vehicle control. The data are presented as relative percentage compared to that of the vehicle control. The p-value was calculated using one-way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05; **, p <0.01, and ***, p <0.001 compared to the control group.
Fig. 3 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 3. Nerolidol treatment led to the generation of intracellular ROS and impaired the mitochondrial membrane potential. (A) ELT3 cells were harvested after trypsin/EDTA treatment and then treated with 20 mM NAC, followed by DCFDA staining for 30 min. The cells were then treated with nerolidol for another additional 30 min, and DCF fluorescence was detected using flow cytometry. H2O2 was used as the positive control. The data were analyzed using the FlowJo software. (B, C) ELT3 cells were harvested and treated with nerolidol for 30 min. The cells were then stained with JC-1 dye for 15 min, followed by flow cytometry analysis. FCCP was used as the positive control. The data were analyzed using the FlowJo software. (B) The gated cells in the graphs indicate the cells with low mitochondrial membrane potential, and the quantitative results are plotted in (C). (D) ELT3 cells were treated with the indicated concentration of nerolidol for 48 h with or without co-treatment with 5 mM NAC. Cell proliferation was determined using the MTT assay. Ethanol (1 %) was used as the vehicle control. The data are presented as relative percentage compared to that of the vehicle control. (E) ELT3 cells were treated with the indicated concentration of nerolidol for 48 h with or without co-treatment with 20 μM ferrostatin-1. Cell proliferation was determined using the MTT assay. Ethanol (1 %) was used as the vehicle control. The data are presented as relative percentage compared to that of the vehicle control. The p-values were calculated using one-way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05; ***, p <0.001 compared to the vehicle control group (C). ***, p <0.001 compared to the nerolidol single treatment group (D, E).
Fig. 4 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 4. Treatment with nerolidol triggered DNA damage in rat leiomyoma cells. (A, B) ELT3 cells were harvested and treated with 100 μM nerolidol for 30 min, followed by determination of DNA damage using the comet assay. H2O2 (200 μM) was used as the positive control. The tail moments are indicated by red arrows in (A), as quantified using a live video imaging system, and dot plots show the mean ± SD in (B). (C, D, E) ELT3 cells were treated with 100 μM nerolidol for 1 h, followed by incubation with anti-p-γH2AXser139 antibody and FITC-conjugated secondary antibody. Nuclei were visualized using DAPI (blue). (C) P-γH2AXser139 expression was quantified using an automated imaging system. The relative positive cell number and the nuclear p-γH2AXser139 intensities are plotted in (D) and (E), respectively. The p-value was calculated using one-way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05; **, p <0.01, and ***, p <0.001 compared to the vehicle control group (1 % EtOH). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Fig. 2. Nerolidol induced G1 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 2. Nerolidol induced G1 cell cycle arrest by downregulating Akt phosphorylation and cell cycle-related proteins. ELT3 cells were treated with the indicated concentrations of nerolidol for 48 h and were then harvested after trypsin/EDTA treatment. (A, B) For cell cycle analysis, the harvested cells were fixed with 70 % ethanol, followed by propidium iodide staining, and the DNA content was measured using flow cytometry. The results were analyzed using the FlowJo software (A). Blue, olive green, and green represent the G1, S, and G2/M phases, respectively. The percentage of each cell cycle phase was plotted in (B). The p-value was calculated using one-way ANOVA with Tukey's multiple post hoc test for each group.*, p <0.05; **, p <0.01, and ***, p <0.001 compared to the vehicle control group (1 % EtOH). (C) Total cellular protein content was measured, and the expression levels of phosphorylated Akt, total Akt, cyclin D1, CDK4, and CDK6 were determined using western blot analysis. β-Actin was used as the loading control. The inserted numbers in (C) indicate the relative expression level compared to that of the vehicle control (indicated as 0 μM). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Fig. 1 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway
Fig. 1. Nerolidol inhibited the proliferation of rat leiomyoma cells. ELT3 cells were seeded in 24-well plates and treated with the indicated concentrations of nerolidol for 48 h. (A) Images were captured under an inverted microscope at 100 × magnification. (B) The cells were trypsinized, and the number of viable (upper panel) or dead (lower panel) cells was counted after staining with trypan blue with a hemocytometer. (C) Cell proliferation was also determined using the MTT assay. Ethanol (1 %) was used as the vehicle control, which is indicated as 0 μM. The data are presented as relative percentage compared to the vehicle control. The p-value was calculated using one way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05 and ***, p <0.001 compared to the vehicle control group. The IC50 values were calculated using the IC50 Calculator (https://www.aatbio.com/tools/ic50-calculator).
The Production of Reactive Oxygen Species in Response to Glutathione Supplementation and Acute Exercise
ClinicalTrials.gov study NCT02948673. IPD Sharing: NO. Countries: 1. Publications: 20.
Inhaled Apocynin Decreases Reactive Oxygen Species Concentrations in Exhaled Breath Condensate in Mild Asthmatics
ClinicalTrials.gov study NCT00992667. IPD Sharing: Not stated. Countries: 1. Publications: 6.
Effect of Thiamine on Serum Glucagon And Reactive Oxygen Species (ROS)
ClinicalTrials.gov study NCT05663164. IPD Sharing: Not stated. Countries: 1. Publications: 9.
Efficacy of Wet Cupping on Reactive Oxygen Species and Antioxidants
ClinicalTrials.gov study NCT03503903. IPD Sharing: NO. Countries: 1. Publications: 3.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
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DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.