Electrochemical Determination of the Superoxide Ion Concentration from KO2 Dissolved in Dimethyl Sulfoxide

Takekawa, Tetsuya; Yamada, Akifumi

doi:10.2116/analsci.20.1465

Cited by 7 publications

(13 citation statements)

References 14 publications

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“…Conversely, exogenous superoxide added in the form of KO 2 52 significantly stimulated cytochrome c release in mitochondria incubated at 39 µmol/l Ca 2+ (fig 6F); ie, in conditions in which ROS production was blocked (fig 6A). Of note, KO 2 had no effect on ΔΨm (data not shown).…”

Section: Resultsmentioning

confidence: 96%

Mechanisms regulating cytochrome c release in pancreatic mitochondria

Odinokova

Sung

Mareninova

et al. 2008

Gut

124

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Background Mechanisms of acinar cell death in pancreatitis are poorly understood. Cytochrome c release is a central event in apoptosis in pancreatitis. Here, we assessed the regulation of pancreatic cytochrome c release by Ca2+, mitochondrial membrane potential (ΔΨm), and reactive oxygen species (ROS), the signals involved in acute pancreatitis. We used both isolated rat pancreatic mitochondria and intact acinar cells hyper-stimulated with cholecystokinin-8 (CCK-8; in vitro model of acute pancreatitis). Results Micromolar amounts of Ca2+ depolarised isolated pancreatic mitochondria through a mechanism different from the “classical” (ie, liver) mitochondrial permeability transition pore (mPTP). In contrast with liver, Ca2+-induced mPTP opening caused a dramatic decrease in ROS and was not associated with pancreatic mitochondria swelling. Importantly, we found that Ca2+-induced depolarisation inhibited cytochrome c release from pancreatic mitochondria, due to blockade of ROS production. As a result, Ca2+ exerted two opposite effects on cytochrome c release: Ca2+ per se stimulated the release, whereas Ca2+-induced depolarisation inhibited it. This dual effect caused a non-monotonous dose-dependence of cytochrome c release on Ca2+. In intact acinar cells, cytochrome c release, caspase activation and apoptosis were all stimulated by ROS and Ca2+, and inhibited by depolarisation, corroborating the findings on isolated pancreatic mitochondria. Conclusions These data implicate ROS as a key mediator of CCK-induced apoptotic responses. The results indicate a major role for mitochondria in the effects of Ca2+ and ROS on acinar cell death. They suggest that the extent of apoptosis in pancreatitis is regulated by the interplay between ROS, ΔΨm and Ca2+. Stabilising mitochondria against loss of ΔΨm may represent a strategy to mitigate the severity of pancreatitis.

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Section: Resultsmentioning

confidence: 96%

Mechanisms regulating cytochrome c release in pancreatic mitochondria

Odinokova

Sung

Mareninova

et al. 2008

Gut

124

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“…! ) concentration is determined by its maximum solubility of ~1 mM in the aprotic solvent 32 (Note that in metal-oxygen batteries, ! !…”

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confidence: 99%

“…Second, electrolyte crystal growth is studied in electrolyte solutions with stoichiometric or near-stoichiometric ratios of the cations and anions. By contrast, in an aprotic metal–oxygen battery, the cation concentration (M + ) is determined by the electrolyte salt concentration, while the anion (O 2 – ) concentration is determined by its maximum solubility of ∼1 mM in the aprotic solvent . (Note that in metal–oxygen batteries, O 2 – is electrochemically generated by the reduction of molecular oxygen during discharge.)…”

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confidence: 99%

Ion Pairing Limits Crystal Growth in Metal–Oxygen Batteries

et al. 2018

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Aprotic alkali metal-oxygen batteries are widely considered to be promising high specific energy alternatives to Li-ion batteries. The growth and dissolution of alkali metal oxides such as Li 2 O 2 in Li-O 2 batteries and NaO 2 and KO 2 in Na-and K-O 2 batteries, respectively, is central to the discharge and charge processes in these batteries. However, crystal growth and dissolution of the discharge products, especially in aprotic electrolytes, is poorly understood. In this work, we chose the growth of NaO 2 in Na-O 2 batteries as a model system and show that there is a strong correlation between the electrolyte salt concentration and the NaO 2 crystal size. With a combination of experiments and theory, we argue that the correlation is a direct manifestation of the strong cation-anion interactions leading to decreased crystal growth rate at high salt concentrations. Further, we propose and experimentallydemonstrate that cation-coordinating crown molecules are suitable electrochemically stable electrolyte additives that weaken ion-pairing and enhance discharge capacities in metal-oxygen batteries while not negatively affecting their rechargeability.

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“…The changes in the both signals were slower and less pronounced when using xanthine/xanthine oxidase as a source of superoxide. In an aqueous solution, potassium superoxide decomposes relatively fast to superoxide radicals, while the enzymatic generation of superoxide is a relatively slow process . Hydrogen peroxide did not change the fluorescent and EPR signals of QD@CD-TEMPOH.…”

Section: Resultsmentioning

confidence: 84%

“…In an aqueous solution, potassium superoxide decomposes relatively fast to superoxide radicals, while the enzymatic generation of superoxide is a relatively slow process. 28 Hydrogen peroxide did not change the fluorescent and EPR signals of QD@CD-TEMPOH. This indicates an interaction of QD@CD-TEMPOH with superoxide, but not with hydrogen peroxide, which is consistent with the generally accepted redox-cycling mechanism of cyclic nitroxides.…”

Section: ■ Results and Discussionmentioning

confidence: 88%

Quantum Sensors To Track Total Redox-Status and Oxidative Stress in Cells and Tissues Using Electron-Paramagnetic Resonance, Magnetic Resonance Imaging, and Optical Imaging

et al. 2021

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Total redox capacity (TRC) and oxidative stress (OxiStress) of biological objects (such as cells, tissues, and body fluids) are some of the most frequently analyzed parameters in life science. Development of highly sensitive molecular probes and analytical methods for detection of these parameters is a rapidly growing sector of BioTech's R&D industry. The aim of the present study was to develop quantum sensors for tracking the TRC and/ or OxiStress in living biological objects using electron-paramagnetic resonance (EPR), magnetic resonance imaging (MRI), and optical imaging. We describe a two-set sensor system: (i) TRC

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Electrochemical Determination of the Superoxide Ion Concentration from KO2 Dissolved in Dimethyl Sulfoxide

Cited by 7 publications

References 14 publications

Mechanisms regulating cytochrome c release in pancreatic mitochondria

Mechanisms regulating cytochrome c release in pancreatic mitochondria

Ion Pairing Limits Crystal Growth in Metal–Oxygen Batteries

Quantum Sensors To Track Total Redox-Status and Oxidative Stress in Cells and Tissues Using Electron-Paramagnetic Resonance, Magnetic Resonance Imaging, and Optical Imaging

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