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Reactive oxygen species in iridium-based OER catalysts.

ABSTRACT: Tremendous effort has been devoted towards elucidating the fundamental reasons for the higher activity of hydrated amorphous Ir^III/IV oxyhydroxides (IrO _x ) in the oxygen evolution reaction (OER) in comparison with their crystalline counterpart, rutile-type IrO₂, by focusing on the metal oxidation state. Here we demonstrate that, through an analogy to photosystem II, the nature of this reactive species is not solely a property of the metal but is intimately tied to the electronic structure of oxygen. We use a combination of synchrotron-based X-ray photoemission and absorption spectroscopies, ab initio calculations, and microcalorimetry to show that holes in the O 2p states in amorphous IrO _x give rise to a weakly bound oxygen that is extremely susceptible to nucleophilic attack, reacting stoichiometrically with CO already at room temperature. As such, we expect this species to play the critical role of the electrophilic oxygen involved in O-O bond formation in the electrocatalytic OER on IrO _x . We propose that the dynamic nature of the Ir framework in amorphous IrO _x imparts the flexibility in Ir oxidation state required for the formation of this active electrophilic oxygen.

SUBMITTER: Pfeifer V

PROVIDER: S-EPMC5134683 | biostudies-literature |

REPOSITORIES: biostudies-literature

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<i>In situ</i> observation of reactive oxygen species forming on oxygen-evolving iridium surfaces.

Project description:Water splitting performed in acidic media relies on the exceptional performance of iridium-based materials to catalyze the oxygen evolution reaction (OER). In the present work, we use in situ X-ray photoemission and absorption spectroscopy to resolve the long-standing debate about surface species present in iridium-based catalysts during the OER. We find that the surface of an initially metallic iridium model electrode converts into a mixed-valent, conductive iridium oxide matrix during the OER, which contains OII- and electrophilic OI- species. We observe a positive correlation between the OI- concentration and the evolved oxygen, suggesting that these electrophilic oxygen sites may be involved in catalyzing the OER. We can understand this observation by analogy with photosystem II; their electrophilicity renders the OI- species active in O-O bond formation, i.e. the likely potential- and rate-determining step of the OER. The ability of amorphous iridium oxyhydroxides to easily host such reactive, electrophilic species can explain their superior performance when compared to plain iridium metal or crystalline rutile-type IrO2.

| S-EPMC5407268 | biostudies-literature

Balancing activity, stability and conductivity of nanoporous core-shell iridium/iridium oxide oxygen evolution catalysts.

Project description:The selection of oxide materials for catalyzing the oxygen evolution reaction in acid-based electrolyzers must be guided by the proper balance between activity, stability and conductivity-a challenging mission of great importance for delivering affordable and environmentally friendly hydrogen. Here we report that the highly conductive nanoporous architecture of an iridium oxide shell on a metallic iridium core, formed through the fast dealloying of osmium from an Ir25Os75 alloy, exhibits an exceptional balance between oxygen evolution activity and stability as quantified by the activity-stability factor. On the basis of this metric, the nanoporous Ir/IrO2 morphology of dealloyed Ir25Os75 shows a factor of ~30 improvement in activity-stability factor relative to conventional iridium-based oxide materials, and an ~8 times improvement over dealloyed Ir25Os75 nanoparticles due to optimized stability and conductivity, respectively. We propose that the activity-stability factor is a key "metric" for determining the technological relevance of oxide-based anodic water electrolyzer catalysts.

| S-EPMC5682288 | biostudies-literature

Reactive Oxygen Species-Regulating Strategies Based on Nanomaterials for Disease Treatment.

Project description:Reactive oxygen species (ROS) play an essential role in physiological and pathological processes. Studies on the regulation of ROS for disease treatments have caused wide concern, mainly involving the topics in ROS-regulating therapy such as antioxidant therapy triggered by ROS scavengers and ROS-induced toxic therapy mediated by ROS-elevation agents. Benefiting from the remarkable advances of nanotechnology, a large number of nanomaterials with the ROS-regulating ability are developed to seek new and effective ROS-related nanotherapeutic modalities or nanomedicines. Although considerable achievements have been made in ROS-based nanomedicines for disease treatments, some fundamental but key questions such as the rational design principle for ROS-related nanomaterials are held in low regard. Here, the design principle can serve as the initial framework for scientists and technicians to design and optimize the ROS-regulating nanomedicines, thereby minimizing the gap of nanomedicines for biomedical application during the design stage. Herein, an overview of the current progress of ROS-associated nanomedicines in disease treatments is summarized. And then, by particularly addressing these known strategies in ROS-associated therapy, several fundamental and key principles for the design of ROS-associated nanomedicines are presented. Finally, future perspectives are also discussed in depth for the development of ROS-associated nanomedicines.

| S-EPMC7856897 | biostudies-literature

Reactive oxygen species enhance insulin sensitivity.

Project description:Chronic reactive oxygen species (ROS) production by mitochondria may contribute to the development of insulin resistance, a primary feature of type 2 diabetes. In recent years it has become apparent that ROS generation in response to physiological stimuli such as insulin may also facilitate signaling by reversibly oxidizing and inhibiting protein tyrosine phosphatases (PTPs). Here we report that mice lacking one of the key enzymes involved in the elimination of physiological ROS, glutathione peroxidase 1 (Gpx1), were protected from high-fat-diet-induced insulin resistance. The increased insulin sensitivity in Gpx1(-/-) mice was attributed to insulin-induced phosphatidylinositol-3-kinase/Akt signaling and glucose uptake in muscle and could be reversed by the antioxidant N-acetylcysteine. Increased insulin signaling correlated with enhanced oxidation of the PTP family member PTEN, which terminates signals generated by phosphatidylinositol-3-kinase. These studies provide causal evidence for the enhancement of insulin signaling by ROS in vivo.

| S-EPMC2892288 | biostudies-literature

How mitochondria produce reactive oxygen species.

Project description:The production of ROS (reactive oxygen species) by mammalian mitochondria is important because it underlies oxidative damage in many pathologies and contributes to retrograde redox signalling from the organelle to the cytosol and nucleus. Superoxide (O2(*-)) is the proximal mitochondrial ROS, and in the present review I outline the principles that govern O2(*-) production within the matrix of mammalian mitochondria. The flux of O2(*-) is related to the concentration of potential electron donors, the local concentration of O2 and the second-order rate constants for the reactions between them. Two modes of operation by isolated mitochondria result in significant O2(*-) production, predominantly from complex I: (i) when the mitochondria are not making ATP and consequently have a high Deltap (protonmotive force) and a reduced CoQ (coenzyme Q) pool; and (ii) when there is a high NADH/NAD+ ratio in the mitochondrial matrix. For mitochondria that are actively making ATP, and consequently have a lower Deltap and NADH/NAD+ ratio, the extent of O2(*-) production is far lower. The generation of O2(*-) within the mitochondrial matrix depends critically on Deltap, the NADH/NAD+ and CoQH2/CoQ ratios and the local O2 concentration, which are all highly variable and difficult to measure in vivo. Consequently, it is not possible to estimate O2(*-) generation by mitochondria in vivo from O2(*-)-production rates by isolated mitochondria, and such extrapolations in the literature are misleading. Even so, the description outlined here facilitates the understanding of factors that favour mitochondrial ROS production. There is a clear need to develop better methods to measure mitochondrial O2(*-) and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.

| S-EPMC2605959 | biostudies-literature

Reactive oxygen species in phagocytic leukocytes.

Project description:Phagocytic leukocytes consume oxygen and generate reactive oxygen species in response to appropriate stimuli. The phagocyte NADPH oxidase, a multiprotein complex, existing in the dissociated state in resting cells becomes assembled into the functional oxidase complex upon stimulation and then generates superoxide anions. Biochemical aspects of the NADPH oxidase are briefly discussed in this review; however, the major focus relates to the contributions of various modes of microscopy to our understanding of the NADPH oxidase and the cell biology of phagocytic leukocytes.

| S-EPMC2491708 | biostudies-other

A Bibliometric Analysis of Reactive Oxygen Species Based Nanotechnology for Cardiovascular Diseases.

Project description:Cardiovascular diseases (CVDs) continue to be the leading cause of health problems around the world. Because of its unique properties, reactive oxygen species (ROS)-based nanotechnology offers novel solutions to the diagnosis and treatment of CVDs. In order to identify and further promote the development of ROS-based nanotechnology in CVDs, we here provide a bibliometric analysis. 701 eligible articles about the ROS-based nanotechnology for CVD up to May 26th, 2022, were taken from the Web of Science Core Collection database. The VOSviewer was used to analyze annual publications, countries/institutions, funding agencies, journals and research category, and the research hotspots. From the publication of the first article in 2005 to 2021, the output and the number of citations of articles are on the rise. Based on the bibliometric analysis, we found that the current research focuses on the correlation between diagnosis (sensors and), treatment (oxidative stress, inflammation, and drug delivery) and safety (toxicity). Since 2019, research on nanomedicine and drug delivery has become a hotspot. So, more research in chemistry, materials, biology, and medicine is required to further develop and construct ROS-based nanomaterials.

| S-EPMC9294284 | biostudies-literature

Reactive oxygen species induced gene expression changes on dendritic cells

Project description:Identification of ROS induced genes on dendritic cells Dendritic cells were incubated for 15 min with or without a ROS inhibitor (DPI), washed extensively and incubated for 30 min with a chemical allergen (DNFB), hydrogen peroxide, and vehicle alone in HBSS containing DPI or vehicle. After washed extensively, the samples were post-incubated for 5.5 h with DNFB, hydrogen peroxide, or vehicle in complete culture medium containing DPI or vehicle.

2011-03-10 | GSE20727 | GEO

Expression Data of Reactive Oxygen Species Signalling in C. elegans

Project description:We have shown that worms that possess mutations in two electron transport chain subunits live longer due to mtROS signalling. Wild type worms can also live longer by treatment with the pro-oxidant paraquat. Paraquat treatment is not additive to the mutations in the ETC subunits. We aimed to determine the underlying changes in gene expression that were common to both paraquat treatment and the two mutations. We also have shown genetically that the mtROS signal that leads to extended lifespan is dependent on CED-4. We generated double mutants that lack functional CED-4 with the two mutations in the ETC subunits. We have found that a large number of gene expression changes by mtROS signalling are reverted by loss of CED-4.

2014-05-08 | GSE54024 | GEO

Reactive oxygen species induced gene expression changes on dendritic cells

2011-03-10 | E-GEOD-20727 | biostudies-arrayexpress

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