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MiRNA species as systemic mediators of environmentally persistent free radical-induced endothelial dysfunction [C57 mice]

ABSTRACT: miRNA species as systemic mediators of environmentally persistent free radical-induced endothelial dysfunction [C57 mice]

PROVIDER: PRJNA1208053 | ENA |

REPOSITORIES: ENA

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miRNA species as systemic mediators of environmentally persistent free radical-induced endothelial dysfunction [C57 mice]

Project description:Plasma miRNA data from particulate matter containing environmentally persistent free radical exposed mice

2025-04-01 | GSE286172 | GEO

miRNA species as systemic mediators of environmentally persistent free radical-induced endothelial dysfunction [Transgenic mice]

Project description:Plasma miRNA data from particulate matter containing environmentally persistent free radical exposed mice

2025-04-01 | GSE286171 | GEO

miRNA species as systemic mediators of environmentally persistent free radical-induced endothelial dysfunction [Transgenic mice]

Project description:miRNA species as systemic mediators of environmentally persistent free radical-induced endothelial dysfunction [Transgenic mice]

| PRJNA1208052 | ENA

Hydroxyl radical generation from environmentally persistent free radicals (EPFRs) in PM2.5.

Project description:Hydroxyl radicals were generated from an aqueous suspension of ambient PM2.5 and detected utilizing 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) as a spin trap coupled with electron paramagnetic resonance (EPR) spectroscopy. Results from this study suggested the importance of environmentally persistent free radicals (EPFRs) in PM2.5 to generate significant levels of ·OH without the addition of H2O2. Particles for which the EPFRs were allowed to decay over time induced less hydroxyl radical. Additionally, higher particle concentrations produced more hydroxyl radical. Some samples did not alter hydroxyl radical generation when the solution was purged by air. This is ascribed to internal, rather than external surface associated EPFRs.

| S-EPMC4308723 | biostudies-literature

Environmentally relevant concentrations of the flame retardant BDE-209 in sediment cause minimal effects on Zebrafish embryos.

Project description:Polychlorinated diphenyl ethers are lipophilic, persistent, and bioaccumulable compounds widely used as flame-retardants. These are chemicals of increasing environmental concern due to their lipophilic, persistent, and bioaccumulable characteristics. The objective of this study was to analyze the potential bioavailability and bioaccumulation of BDE-209 as a source of toxicity. Zebrafish embryos were exposed for 8 days to sediments spiked with an environmentally relevant concentration of BDE-209. We analyzed gene expression changes, thyroid function, and several markers for neurotoxicity. Results of this research highlight the need to consider the capability of BDE-209 to be bioavailable and bioaccumulate, indicating the potential hazardous effects.

2013-01-01 | GSE39169 | GEO

Hydrogen modulates signal transduction through manipulating oxidized phospholipid mediators

Project description:We have previously demonstrated that molecular hydrogen (H2) neutralizes hydroxyl radical (•OH) in cultured-cells and protects cells and tissues against oxidative stress. Growing evidence has confirmed that H2-consumption exhibits preventive and therapeutic effects in patients with various diseases as well as model animals. Moreover, a small amount of H2 modulates signal transduction for regulating the expression of various genes; however, the primary target of H2 for exhibiting a variety of phenotypes was completely unknown. Here we show that H2 at low amounts manipulates oxidized phospholipid mediators to modulate Ca2+-signal transduction and gene expression.

2014-10-17 | GSE62434 | GEO

A critical review of environmentally persistent free radical (EPFR) solvent extraction methodology and retrieval efficiency.

Project description:Long-lived environmentally persistent free radical (EPFR) exposures have been shown in toxicology studies to lead to respiratory and cardiovascular effects, which were thought to be due to the persistence of EPFR and their ability to produce reactive oxygen species. To characterize EPFR exposure and resulting health impacts, it is necessary to identify and systematize analysis protocols. Both direct measurement and solvent extraction methods have been applied to analyze environmental samples containing EPFR. The use of different protocols and solvents in EPFR analyses makes it difficult to compare results among studies. In this work, we reviewed EPFR studies that involved solvent extraction and carefully reported the details of the extraction methodology and retrieval recovery. EPFR recovery depends on the structure of the radical species and the solvent. For the limited number of studies available for review, the polar solvents had superior recovery in more studies. Radicals appeared to be more oxygen-centered following extraction for fly ash and particulate matter (PM) samples. Different solvent extraction methods to retrieve EPFR may produce molecular products during the extraction, thus potentially changing the sample toxicity. The number of studies reporting detailed methodologies is limited, and data in these studies were not consistently reported. Thus, inference about the solvent and protocol that leads to the highest EPFR extraction efficiency for certain types of radicals is not currently possible. Based on our review, we proposed reporting criteria to be included for future EPFR studies.

| S-EPMC8487994 | biostudies-literature

Astaxanthin protects against environmentally persistent free radical-induced oxidative stress in well-differentiated respiratory epithelium.

Project description:Environmentally persistent free radicals (EPFRs) are combustion products present in substantial numbers on atmospheric particulate matter with half-lives of days to years. The mechanisms linking EPFR exposure and respiratory diseases are unclear, but likely involve oxidative stress. We investigated the mechanisms by which EPFR exposure impact on well-differentiated primary human nasal epithelial cells from subjects sensitive or resistant to oxidant stressors, cultured at an air-liquid interface. We found that EPFR exposure induced mitochondrial reactive oxygen species (mtROS) production; increased mitochondrial DNA copy number; down-regulated mucus production gene, Mucin-5AC (MUC5AC); up-regulated detoxifying gene, cytochrome P450 1A1 (CYP1A1), nuclear factor erythroid 2-related factor 2 (NRF2)-regulated antioxidant pathways including Sirtuin 1 (SIRT1)-Forkhead box O3 (FOXO3), mitophagy, PTEN-induced kinase 1 (PINK1), apoptosis, cyclin-dependent kinase inhibitor p21 (p21), and inflammation, C-C motif chemokine ligand 5 (CCL5). These results indicate that the well-differentiated respiratory epithelium can respond and activate redox reactions when exposed to sublethal concentrations of EPFRs. Increased susceptibility to EPFR exposure is conferred by failure to upregulate the mucin gene, MUC5AC, expression. Pre-treatment with astaxanthin prevented most of the negative impacts caused by EPFRs. Our results demonstrate that EPFRs can induce oxidative stress and cause damage to respiratory epithelium. A dietary antioxidant, astaxanthin, protected cells from EPFR-induced oxidant stress.

| S-EPMC11875192 | biostudies-literature

C57 versus NZBW

Project description:Gene expression studies in B-1 cells from lupus-prone mice versus C57/Bl6 mice (control)

2015-04-03 | E-MEXP-3598 | biostudies-arrayexpress

Hydrogen modulates signal transduction through manipulating oxidized phospholipid mediators

Project description:We have previously demonstrated that molecular hydrogen (H2) neutralizes hydroxyl radical (M-bM-^@M-"OH) in cultured-cells and protects cells and tissues against oxidative stress. Growing evidence has confirmed that H2-consumption exhibits preventive and therapeutic effects in patients with various diseases as well as model animals. Moreover, a small amount of H2 modulates signal transduction for regulating the expression of various genes; however, the primary target of H2 for exhibiting a variety of phenotypes was completely unknown. Here we show that H2 at low amounts manipulates oxidized phospholipid mediators to modulate Ca2+-signal transduction and gene expression. Gene expression was measured at 4 hours after exposure to phospholipid, PAPC or oxidized PAPC that had been air-oxidized for 3 days with 0, 1.3 or 5% H2. Three independent experiments were performed for each experiment.

2014-10-17 | E-GEOD-62434 | biostudies-arrayexpress

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