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Redox Cycling (redox + cycling)
Selected AbstractsRedox Cycling of Ni-Based Solid Oxide Fuel Cell Anodes: A ReviewFUEL CELLS, Issue 3 2007D. Sarantaridis Abstract The published literature relating to damage to SOFCs caused by redox cycling of Ni-based anodes is reviewed. The review covers the kinetics of Ni oxidation and NiO reduction (as single phases and as constituents of composites with yttria-stabilised zirconia, YSZ), the dimensional changes associated with redox cycling and the effect of this on the mechanical integrity and electrical performance of cells and stacks. A critical parameter is the expansion strain that is caused by oxidation. Several studies report that the first complete oxidation of a Ni/YSZ composite causes a linear expansion of the order of 1%, but the actual values vary substantially between different investigations. The oxidation strain is the result of microstructural irreversibility during the redox process and leads to strain accumulation over several redox cycles. This can cause mechanical disruption to an anode, anode support or other cell components attached to the anode. A simplified mechanical model of the stress and damage that are likely to be caused by anode expansion is proposed and applied to anode-supported, electrolyte-supported and inert substrate-supported cell configurations. This allows the maximum oxidation strain to avoid damage in each configuration to be estimated. [source] Ni,YSZ Solid Oxide Fuel Cell Anode Behavior Upon Redox Cycling Based on Electrical CharacterizationJOURNAL OF THE AMERICAN CERAMIC SOCIETY, Issue 11 2007Trine Klemensų Nickel (Ni),yttria-stabilized zirconia (YSZ) cermets are a prevalent material used for solid oxide fuel cells. The cermet degrades upon redox cycling. The degradation is related to microstructural changes, but knowledge of the mechanisms has been limited. Direct current conductivity measurements were performed on cermets and cermets where the Ni component was removed. Measurements were carried out before, during, and after redox cycling the cermet. The cermet conductivity degraded over time due to sintering of the nickel phase. Following oxidizing events, the conductivity of the cermets improved, whereas the conductivity of the YSZ phase decreased. An improved model of the redox degradation mechanism was established based on the measurements. [source] Redox Properties of the Iron Complexes of Orally Active Iron Chelators CP20, CP502, CP509, and ICL670HELVETICA CHIMICA ACTA, Issue 12 2004Martin Merkofer Redox cycling of iron is a critical aspect of iron toxicity. Reduction of a low-molecular-weight iron(III)-complex followed by oxidation of the iron(II)-complex by hydrogen peroxide may yield the reactive hydroxyl radical (OH.) or an oxoiron(IV) species (the Fenton reaction). Complexation of iron by a ligand that shifts the electrode potential of the complex to either to far below ,350,mV (dioxygen/superoxide, pH=7) or to far above +320,mV (H2O2/HO., H2O pH=7) is essential for limitting Fenton reactivity. The oral chelating agents CP20, CP502, CP509, and ICL670 effectively remove iron from patients suffering from iron overload. We measured the electrode potentials of the iron(III) complexes of these drugs by cyclic voltammetry with a mercury electrode and determined the dependence on concentration, pH, and stoichiometry. The standard electrode potentials measured are ,620,mV, ,600,mV, ,535,mV, and ,535,mV with iron bound to CP20, ICL670, CP502, and CP509, respectively, but, at lower chelator concentrations, electrode potentials are significantly higher. [source] Characterization of Nanopore Electrode Structures as Basis for Amplified Electrochemical AssaysELECTROANALYSIS, Issue 19-20 2006Sebastian Neugebauer Abstract A nanopore electrode structure was fabricated consisting of ensembles of nanopores with separately addressable electrodes at the pore bottoms and the rims. A metal/insulator/metal layer structure allowed for adjusting the spacing between the bottom and rim electrodes to be in the range of about 200,nm. Pore diameters varied between 200 and 800,nm. The electrochemical properties of this electrode structure and its perspectives for applications in bioelectronics were studied using cyclic voltammetry and chronoamperometry along with high-resolution scanning electrochemical microscopy (SECM) in constant-distance mode. It was possible to visualize the electrochemical activity of a single nanometric electrode using high-resolution SECM in a combination of sample-generation-tip-collection mode and positive feedback mode. The SECM images suggested an influence of the unbiased rim electrode on redox amplification which was used as a basis for evaluating the feasibility of current amplification by means of redox cycling between the bottom and rim electrodes. Amplification factors superior to those obtained with interdigitated array electrodes could be demonstrated. [source] Comparative mutagenic effects of structurally similar flavonoids quercetin and taxifolin on tester strains Salmonella typhimurium TA102 and Escherichia coli WP-2 uvrAENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 6 2009Patrudu S. Makena Abstract Quercetin (QT) and Taxifolin (TF) are structurally similar plant polyphenols. Both have been reported to have therapeutic potential as anti-cancer drugs and antioxidants. Mutagenic effects of QT and TF were evaluated using Salmonella typhimurium TA102 and Escherichia coli WP-2 uvrA tester strains. Either in the presence or absence of S9 mix, QT was mutagenic to TA102 and WP2 uvrA. However, the mutagenicity of QT was significantly enhanced in the presence of S9 mix. Likewise, in the presence of Iron (Fe2+) and NADPH generating system (NGS) and absence of S9 mix, QT induced significantly high mutations in both TA102 and WP-2 uvrA. Mutagenicity of QT decreased in both strains in the presence of Iron (Fe2+) or NGS alone. TF was not mutagenic in the presence or absence of S9 mix in both TA102 and WP-2 uvrA 2, regardless of the presence of iron or NGS. Incorporation of antioxidants (ascorbate, superoxide dismutase (SOD), catalase (CAT)) and/or iron chelators (desferroxamine (DF) and ethylenediamine-tetraacetate (EDTA)) in the test systems markedly decreased QT-induced mutations in both tester strains. These results suggest that QT but not TF, could induce mutations in the presence or absence of rat liver S9 or Iron (Fe2+) and NGS in both tester strains by redox cycling and Fenton reactions to produce oxygen free radicals. Our results indicate that a minor structural variation between the two plant polyphenols could elicit a marked difference in their genotoxicities. These results provide a basis for further study into the potential use of QT in combination with iron supplements. Environ. Mol. Mutagen. 2009. © 2009 Wiley-Liss, Inc. [source] Anaerobic redox cycling of iron by freshwater sediment microorganismsENVIRONMENTAL MICROBIOLOGY, Issue 1 2006Karrie A. Weber Summary The potential for microbially mediated anaerobic redox cycling of iron (Fe) was examined in a first-generation enrichment culture of freshwater wetland sediment microorganisms. Most probable number enumerations revealed the presence of significant populations of Fe(III)-reducing (approximately 108 cells ml,1) and Fe(II)-oxidizing, nitrate-reducing organisms (approximately 105 cells ml,1) in the freshwater sediment used to inoculate the enrichment cultures. Nitrate reduction commenced immediately following inoculation of acetate-containing (approximately 1 mM) medium with a small quantity (1% v/v) of wetland sediment, and resulted in the transient accumulation of NO2, and production of a mixture of gaseous end-products (N2O and N2) and NH4+. Fe(III) oxide (high surface area goethite) reduction took place after NO3, was depleted and continued until all the acetate was utilized. Addition of NO3, after Fe(III) reduction ceased resulted in the immediate oxidation of Fe(II) coupled to reduction of NO3, to NH4+. No significant NO2, accumulation was observed during nitrate-dependent Fe(II) oxidation. No Fe(II) oxidation occurred in pasteurized controls. Microbial community structure in the enrichment was monitored by denaturing gradient gel electrophoresis analysis of polymerase chain reaction-amplified 16S rDNA and reverse transcription polymerase chain reaction-amplified 16S rRNA, as well as by construction of 16S rDNA clone libraries for four different time points during the experiment. Strong similarities in dominant members of the microbial community were observed in the Fe(III) reduction and nitrate-dependent Fe(II) oxidation phases of the experiment, specifically the common presence of organisms closely related (, 95% sequence similarity) to the genera Geobacter and Dechloromonas. These results indicate that the wetland sediments contained organisms such as Geobacter sp. which are capable of both dissimilatory Fe(III) reduction and oxidation of Fe(II) with reduction of NO3, to NH4+. Our findings suggest that microbially catalysed nitrate-dependent Fe(II) oxidation has the potential to contribute to a dynamic anaerobic Fe redox cycle in freshwater sediments. [source] Fatty acids increase the circulating levels of oxidative stress factors in mice with diet-induced obesity via redox changes of albuminFEBS JOURNAL, Issue 15 2007Mayumi Yamato Plasma concentrations of free fatty acids are increased in metabolic syndrome, and the increased fatty acids may cause cellular damage via the induction of oxidative stress. The present study was designed to determine whether the increase in fatty acids can modify the free sulfhydryl group in position 34 of albumin (Cys34) and enhance the redox-cycling activity of the copper,albumin complex in high-fat diet-induced obese mice. The mice were fed with commercial normal diet or high-fat diet and water ad libitum for 3 months. The high-fat diet-fed mice developed obesity, hyperlipemia, and hyperglycemia. The plasma fatty acid/albumin ratio also significantly increased in high-fat diet-fed mice. The increased fatty acid/albumin ratio was associated with conformational changes in albumin and the oxidation of sulfhydryl groups. Moreover, an ascorbic acid radical, an index of redox-cycling activity of the copper,albumin complex, was detected only in the plasma from obese mice, whereas the plasma concentrations of ascorbic acid were not altered. Plasma thiobarbituric acid reactive substances were significantly increased in the high-fat diet group. These results indicate that the increased plasma fatty acids in the high-fat diet group resulted in the activated redox cycling of the copper,albumin complex and excessive lipid peroxidation. [source] Redox Cycling of Ni-Based Solid Oxide Fuel Cell Anodes: A ReviewFUEL CELLS, Issue 3 2007D. Sarantaridis Abstract The published literature relating to damage to SOFCs caused by redox cycling of Ni-based anodes is reviewed. The review covers the kinetics of Ni oxidation and NiO reduction (as single phases and as constituents of composites with yttria-stabilised zirconia, YSZ), the dimensional changes associated with redox cycling and the effect of this on the mechanical integrity and electrical performance of cells and stacks. A critical parameter is the expansion strain that is caused by oxidation. Several studies report that the first complete oxidation of a Ni/YSZ composite causes a linear expansion of the order of 1%, but the actual values vary substantially between different investigations. The oxidation strain is the result of microstructural irreversibility during the redox process and leads to strain accumulation over several redox cycles. This can cause mechanical disruption to an anode, anode support or other cell components attached to the anode. A simplified mechanical model of the stress and damage that are likely to be caused by anode expansion is proposed and applied to anode-supported, electrolyte-supported and inert substrate-supported cell configurations. This allows the maximum oxidation strain to avoid damage in each configuration to be estimated. [source] Redox-Tunable Defects in Colloidal Photonic Crystals,ADVANCED MATERIALS, Issue 20 2005F. Fleischhaker Reversible tuning of an intragap transmitting state induced by redox cycling is accomplished using a redox-active polyelectrolyte multilayer planar defect embedded in a colloidal photonic crystal (CPC). The wavelength position of the defect state can be changed by changing the oxidation state of the ferrocene moieties in the polymer backbone (see Figure). This could find applications in electrochemically tunable microcavities and CPC-based laser sources. [source] Human Heart Cytosolic Reductases and Anthracycline CardiotoxicityIUBMB LIFE, Issue 1 2001Alvaro Mordente Abstract Anthracyclines are a class of antitumor drugs widely used for the treatment of a variety of malignancy, including leukemias, lymphomas, sarcomas, and carcinomas. Different mechanisms have been proposed for anthracycline antitumor effects including freeradical generation, DNA intercalation/binding, activation of signaling pathways, inhibition of topoisomerase II and apoptosis. A life-threatening form of cardiomyopathy hampers the clinical use of anthracyclines. According to the prevailing hypothesis, anthracyclines injure the heart by generating damaging free radicals through iron-catalyzed redox cycling. Although the "iron and freeradical hypothesis" can explain some aspects of anthracycline acute toxicity, it is nonetheless disappointing when referred to chronic cardiomyopathy. An alternative hypothesis implicates C-13 alcohol metabolites of anthracyclines as mediators of myocardial contractile dysfunction ("metabolite hypothesis"). Hydroxy metabolites are formed upon two-electron reduction of the C-13 carbonyl group in the side chain of anthracyclines by cytosolic NADPH-dependent reductases. Anthracycline alcohol metabolites can affect myocardial energy metabolism, ionic gradients, and Ca 2+ movements, ultimately impairing cardiac contraction and relaxation. In addition, alcohol metabolites can impair cardiac intracellular iron handling and homeostasis, by delocalizing iron from the [4Fe-4S] cluster of cytoplasmic aconitase. Chronic cardiotoxicity induced by C-13 alcohol metabolite might be primed by oxidative stress generated by anthracycline redox cycling ("unifying hypothesis"). Putative cardioprotective strategies should be aimed at decreasing C-13 alcohol metabolite production by means of efficient inhibitors of anthracycline reductases, as short-chain coenzyme Q analogs and chalcones that compete with anthracyclines for the enzyme active site, or by developing novel anthracyclines less susceptible to reductive metabolism. [source] Cytotoxic effects of polychlorinated biphenyl hydroquinone metabolites in rat hepatocytesJOURNAL OF APPLIED TOXICOLOGY, Issue 2 2010Katie Chan Abstract Polychlorinated biphenyls (PCBs) are persistent organic pollutants that exhibit various toxic effects in animals and exposed human populations. The molecular mechanisms of PCB toxicity have been attributed to the toxicological properties of its metabolites, such as hydroquinones, formed by cytochrome-P-450 oxidation. The effects of PCB hydroquinone metabolites towards freshly isolated rat hepatocytes were investigated. Hydroquinones can be oxidized to semiquinones and/or quinone metabolites. These metabolites can conjugate glutathione or can oxidize glutathione as a result of redox cycling. This depletes hepatocyte glutathione, which can inhibit cellular defence mechanisms, causing cell death and an increased susceptibility to oxidative stress. However in the following, glutathione-depleted hepatocytes became more resistant to the hydroquinone metabolites of PCBs. This suggested that their glutathione conjugates were toxic and that there was a third type of quinone toxicity mechanism which involved a hydrogen peroxide-accelerated autoxidation of the hydroquinones to form toxic electrophilic quinone and semiquinone,glutathione conjugates. Copyright © 2009 John Wiley & Sons, Ltd. [source] Evidence for redox cycling of lawsone (2-hydroxy-1,4-naphthoquinone) in the presence of the hypoxanthine/xanthine oxidase systemJOURNAL OF APPLIED TOXICOLOGY, Issue 4 2003A. M. Osman Abstract This study reports that lawsone (2-hydroxy-1,4-naphthoquinone) undergoes redox cycling in the presence of the hypoxanthine/xanthine oxidase system. The rate of cytochrome c reduction obtained in the presence of 80 µM lawsone was almost three times the rate of cytochrome c reduction measured in its absence. This increase in the rate of cytochrome c reduction was partially inhibited by superoxide dismutase, suggesting the involvement of O2,, in this process. It is remarkable to note that, even though lawsone is considered to be a non-redox-cycling quinone in vitro, this quinone was shown to be more toxic in vivo in rats than menadione, causing haemolytic anemia of an oxidative nature and renal damage. The view that this quinone is a non-redox-cycling quinone was based on the inability of one-electron-transferring ,avoenzymes such as NADPH-cytochrome c reductase to reduce this naphthoquinone. Our ,nding that lawsone, like menadione, undergoes redox cycling in the presence of the hypoxanthine/xanthine oxidase system could explain the observed oxidative damage of tissues in,icted by this quinone in rats in vivo. Such an observation therefore reconciles the in vivo toxicity results of this naphthoquinone with those of in vitro experiments. Copyright © 2003 John Wiley & Sons, Ltd. [source] Ni,YSZ Solid Oxide Fuel Cell Anode Behavior Upon Redox Cycling Based on Electrical CharacterizationJOURNAL OF THE AMERICAN CERAMIC SOCIETY, Issue 11 2007Trine Klemensų Nickel (Ni),yttria-stabilized zirconia (YSZ) cermets are a prevalent material used for solid oxide fuel cells. The cermet degrades upon redox cycling. The degradation is related to microstructural changes, but knowledge of the mechanisms has been limited. Direct current conductivity measurements were performed on cermets and cermets where the Ni component was removed. Measurements were carried out before, during, and after redox cycling the cermet. The cermet conductivity degraded over time due to sintering of the nickel phase. Following oxidizing events, the conductivity of the cermets improved, whereas the conductivity of the YSZ phase decreased. An improved model of the redox degradation mechanism was established based on the measurements. [source] Melanin as a Target for Melanoma Chemotherapy: Pro-oxidant Effect of Oxygen and Metals on Melanoma ViabilityPIGMENT CELL & MELANOMA RESEARCH, Issue 3 2003Patrick J. Farmer Melanoma cells have a poor ability to mediate oxidative stress, which may be attributed to constitutive abnormalities in their melanosomes. We hypothesize that disorganization of the melanosomes will allow chemical targeting of the melanin within. Chemical studies show that under oxidative conditions, synthetic melanins demonstrate increased metal affinity and a susceptibility to redox cycling with oxygen to form reactive oxygen species. The electron paramagnetic resonance (EPR)-active 5,5,-dimethyl-pyrollidine N-oxide spin adduct was used to show that binding of divalent Zn or Cu to melanin induces a pro-oxidant response under oxygen, generating superoxide and hydroxyl radicals. A similar pro-oxidant behaviour is seen in melanoma cell lines under external peroxide stress. Melanoma cultures grown under 95% O2/5% CO2 atmospheres show markedly reduced viability as compared with normal melanocytes. Cu- and Zn-dithiocarbamate complexes, which induce passive uptake of the metal ions into cells, show significant antimelanoma activity. The antimelanoma effect of metal- and oxygen-induced stress appears additive rather than synergistic; both treatments are shown to be significantly less toxic to melanocytes. [source] Progress in Parasitic Plant Biology: Host Selection and Nutrient TransferPLANT BIOLOGY, Issue 2 2006H. Shen Abstract: Host range varies widely among species of parasitic plants. Parasitic plants realize host selection through induction by chemical molecular signals, including germination stimulants and haustoria-inducing factors (HIFs). Research on parasitic plant biology has provided information on germination, haustorium induction, invasion, and haustorial structures and functions. To date, some molecular mechanisms have been suggested to explain how germination stimulants work, involving a chemical change caused by addition of a nucleophilic protein receptor, and direct or indirect stimulation of ethylene generation. Haustorium initiation is induced by HIFs that are generated by HIF-releasing enzymes from the parasite or triggered by redox cycling between electrochemical states of the inducers. Haustorium attachment is non-specific, however, the attachment to a host is facilitated by mucilaginous substances produced by haustorial hairs. Following the attachment, the intrusive cells of parasites penetrate host cells or push their way through the host epidermis and cortex between host cells, and some types of cell wall-degrading enzymes may assist in the penetration process. After the establishment of host-parasite associations, parasitic plants develop special morphological structures (haustoria) and physiological characteristics, such as high transpiration rates, high leaf conductance, and low water potentials in hemiparasites, for nutrient transfer and resource acquisition from their hosts. Therefore, they negatively affect the growth and development and even cause death of their hosts. [source] Novel structural features in the GMC family of oxidoreductases revealed by the crystal structure of fungal aryl-alcohol oxidaseACTA CRYSTALLOGRAPHICA SECTION D, Issue 11 2009Israel S. Fernįndez Lignin biodegradation, a key step in carbon recycling in land ecosystems, is carried out by white-rot fungi through an H2O2 -dependent process defined as enzymatic combustion. Pleurotus eryngii is a selective lignin-degrading fungus that produces H2O2 during redox cycling of p -anisylic compounds involving the secreted flavoenzyme aryl-alcohol oxidase (AAO). Here, the 2.4,Å resolution X-ray crystal structure of this oxidoreductase, which catalyzes dehydrogenation reactions on various primary polyunsaturated alcohols, yielding the corresponding aldehydes, is reported. The AAO crystal structure was solved by single-wavelength anomalous diffraction of a selenomethionine derivative obtained by Escherichia coli expression and in vitro folding. This monomeric enzyme is composed of two domains, the overall folding of which places it into the GMC (glucose,methanol,choline oxidase) oxidoreductase family, and a noncovalently bound FAD cofactor. However, two additional structural elements exist in the surroundings of its active site that modulate the access of substrates; these are absent in the structure of the model GMC oxidoreductase glucose oxidase. The folding of these novel elements gives rise to a funnel-like hydrophobic channel that connects the solvent region to the buried active-site cavity of AAO. This putative active-site cavity is located in front of the re side of the FAD isoalloxazine ring and near two histidines (His502 and His546) that could contribute to alcohol activation as catalytic bases. Moreover, three aromatic side chains from two phenylalanines (Phe397 and Phe502) and one tyrosine (Tyr92) at the inner region of the channel form an aromatic gate that may regulate the access of the enzyme substrates to the active site as well as contribute to the recognition of the alcohols that can effectively be oxidized by AAO. [source] | ||||||||||||||||