Formation Of Radical Oxygen Species Research Articles

Interfacial Mo, W-Conjugated Polarization, and Oxygen Vacancies of MoO2/WO3 in Enhanced Microwave Therapy for MRSA-Induced Osteomyelitis.

Deep tissue infection, such as osteomyelitis, caused by methicillin-resistant Staphylococcus aureus (MRSA) infection, poses a serious threat to public health and cannot be effectively treated by antibiotics. In this study, we report a microwave (MW)-responsive MoO2/WO3 heterojunction that can be utilized to effectively treat MRSA-infected osteomyelitis under MW irradiation because of the enhanced MW thermal effect and MW catalysis of the composite. The underlying mechanism is as follows: A myriad of oxygen vacancies forms on the surface of MoO2 and WO3 by deoxidization effect with hydrogen from the decomposition of sodium borohydride, which induces a mass of free electrons on the surface of the composite and consequently promotes a localized surface plasmon resonance effect (LSPR) under MW irradiation. Furthermore, the conjugation of Mo and W at the interface enhances the LSPR effect. Thus, the LSPR effect not only induces the formation of radical oxygen species, thereby enhancing MW catalysis, but also results in the formation of an interfacial electrical field, which strengthens dipole polarization through synergistic action with oxygen vacancies and contributes to better MW thermal effects. The characteristics of MoO2/WO3 prove to be promising for the treatment of deep-tissue infections under MW irradiation.

The Pomace Extract Taurisolo Protects Rat Brain From Ischemia-Reperfusion Injury.

Taurisolo® is a pomace extract from Aglianico Grapes, a wine cultivar native to Campania (Southern Italy). It exhibits a very high polyphenolic content and, consumed as a nutraceutical, is effective in reducing the level of Trimethylamine N-oxide (TMAO), a cardiovascular disease risk factor marker. We here show the effects of Taurisolo® on rat brain microvascular alterations induced by a diminution in cerebral blood flow (CBFD) for 30 min, due to bilateral common carotid artery occlusion, and subsequent blood flow restoration (CBFR) for 60 min. The rat pial microcirculation was investigated by intravital fluorescence microscopy through a parietal closed window implanted into the skull bone. The rat pial arterioles were classified according to Strahler’s ordering scheme, from smaller penetrating arterioles up to the larger ones. Western blotting analysis and mass spectrometry (MS)-based metabolomics were used to investigate the expression of endothelial nitric oxide synthase (eNOS) or the presence of peroxidized cardiolipin and several inflammatory mediators, respectively. Radical Oxygen Species (ROS) formation and neuronal loss were assessed. In rats CBFD and CBFR caused a decrease in arteriolar diameter, increase in fluorescent leakage and in adhesion of leukocytes to venular walls, reduction in the length of perfused capillaries and increment of ROS formation with large infarct size. Taurisolo®, intravenously or orally administered, induced pial arteriolar dilation (up to >30% of baseline), prevented fluorescent leakage, adhesion of leukocytes, ROS formation, while facilitated capillary perfusion and significantly reduced infarct size. These effects were accompanied by an increase in eNOS expression. Mass-spectrometry metabolomics analysis detected a marked decrease in the amount of peroxidized cardiolipin and pronounced reduction in pro-inflammatory prostaglandins and thromboxane Txb2. Altogether, these results extend the nutraceutical potential of Taurisolo® and suggest their eligibility for preventing brain damage due to ischemia-reperfusion injury.

Degradation of organic compounds during the corrosion of ZVI by hydrogen peroxide at neutral pH: Kinetics, mechanisms and effect of corrosion promoting and inhibiting ions

The corrosion of zero valent iron (ZVI) by hydrogen peroxide (H2O2) generates hydroxyl (⋅OH) and other radical oxygen species (ROS) that degrade organic materials. To better understand the factors that govern the ROS formation during the H2O2-induced corrosion, we investigated the degradation of an organic probe compound (acesulfame (ACE)) in slurries of ZVI powder in unbuffered laboratory water at pH 6.5 ± 0.5. Chloride ions accelerated the corrosion of ZVI by H2O2 and the formation ROS and, therefore, the degradation of organic materials. Conversely, slowing corrosion by phosphate buffer inhibited ROS formation and the degradation of organic compounds. The rate of H2O2 decomposition was correlated with the liberation of Fe2+(aq) and the ACE degradation rate. The kinetics of H2O2 decomposition was pseudo-first-order and zero-order at low (<0.04 mM/mg) and high [H2O2]/[ZVI] initial ratios, respectively, and was consistent with Langmuir kinetics. The H2O2 decomposition rate was proportional to the ZVI reactive surface area (SA) and nearly independent of the extent of ZVI oxidation, the presence of a Fe2+(aq) chelating agent, and ⋅OH quenchers (methanol and tert-butanol). Kinetic data suggest a mechanism involving rapid cathodic reduction of H2O2 at the metallic ZVI surface which causes the liberation of Fe2+(aq) that generate ⋅OH via the homogeneous Fenton reaction. The stoichiometric efficiency (SE) of organics degradation ranged from 0.0008% to 0.014% and increased with decreasing H2O2 decomposition rate.

Brain inflammasomes in stroke and depressive disorders: Regulation by oestrogen.

Neuroinflammation is a devastating pathophysiological process that results in brain damage and neuronal death. Pathogens, cell fragments and cellular dysfunction trigger inflammatory responses. Irrespective of the cause, inflammasomes are key intracellular multiprotein signalling platforms that sense neuropathological conditions. The activation of inflammasomes leads to the auto-proteolytic cleavage of caspase-1, resulting in the proteolysis of the pro-inflammatory cytokines interleukin (IL)1β and IL18 into their bioactive forms. It also initiates pyroptosis, a type of cell death. The two cytokines contribute to the pathogenesis in acute and chronic brain diseases and also play a central role in human aging and psychiatric disorders. Sex steroids, in particular oestrogens, are well-described neuroprotective agents in the central nervous system. Oestrogens improve the functional outcome after ischaemia and traumatic brain injury, reduce neuronal death in Parkinson's and Alzheimer's disease, as well as in amyotrophic lateral sclerosis, attenuate glutamate excitotoxicity and the formation of radical oxygen species, and lessen the spread of oedema after damage. Moreover, oestrogens alleviate menopause-related depressive symptoms and have a positive influence on depressive disorders probably by influencing growth factor production and serotonergic brain circuits. Recent evidence also suggests that inflammasome signalling affects anxiety- and depressive-like behaviour and that oestrogen ameliorates depression-like behaviour through the suppression of inflammasomes. In the present review, we highlight the most recent findings demonstrating that oestrogens selectively suppress the activation of the neuroinflammatory cascade in the brain in acute and chronic brain disease models. Furthermore, we aim to describe putative regulatory signalling pathways involved in the control of inflammasomes. Finally, we consider that psychiatric disorders such as depression also contain an inflammatory component that could be modulated by oestrogen.

Caffeic Acid Phenethyl Ester Regulates PPAR’s Levels in Stem Cells-Derived Adipocytes

Hypertrophic obesity inhibits activation of peroxisome proliferators-activated receptor gamma (PPARγ), considered the key mediator of the fully differentiated and insulin sensitive adipocyte phenotype. We examined the effects of Caffeic Acid Phenethyl Ester (Cape), isolated from propolis, a honeybee hive product, on Adipose Stem Cells (ASCs) differentiation to the adipocyte lineage. Finally we tested the effects of Cape on insulin-resistant adipocytes. Quantification of Oil Red O-stained cells showed that lipid droplets decreased following Cape treatment as well as radical oxygen species formation. Additionally, exposure of ASC to high glucose levels decreased adiponectin and increased proinflammatory cytokines mRNA levels, which were reversed by Cape-mediated increase of insulin sensitivity. Cape treatment resulted in decreased triglycerides synthesis and increased beta-oxidation. Exposure of ASCs to Lipopolysaccharide (LPS) induced a reduction of PPARγ, an increase of IL-6 levels associated with a well-known stimulation of lipolysis; Cape partially attenuated the LPS-mediated effects. These observations reveal the main role of PPARγ in the adipocyte function and during ASC differentiation. As there is now substantial interest in functional food and nutraceutical products, the observed therapeutic value of Cape in insulin-resistance related diseases should be taken into consideration.

Selective in vitro anticancer effect of superparamagnetic iron oxide nanoparticles loaded in hyaluronan polymeric micelles.

Due to its native origin, excellent biocompatibility and biodegradability, hyaluronan (HA) represents an attractive polymer for superparamagnetic iron oxide nanoparticles (SPION) coating. Herein, we report HA polymeric micelles encapsulating oleic acid coated SPIONs, having a hydrodynamic size of about 100 nm and SPION loading capacity of 1-2 wt %. The HA-SPION polymeric micelles were found to be selectively cytotoxic toward a number of human cancer cell lines, mainly those of colon adenocarcinoma (HT-29). The selective inhibition of cell growth was even observed when the SPION loaded HA polymeric micelles were incubated with a mixture of control and cancer cells. The selective in vitro inhibition could not be connected with an enhanced CD44 uptake or radical oxygen species formation and was rather connected with a different way of SPION intracellular release. While aggregated iron particles were visualized in control cells, nonaggregated solubilized iron oxide particles were detected in cancer cells. In vivo SPION accumulation in intramuscular tumor following an intravenous micelle administration was confirmed by magnetic resonance (MR) imaging and histological analysis. Having a suitable hydrodynamic size, high magnetic relaxivity, and being cancer specific and able to accumulate in vivo in tumors, SPION-loaded HA micelles represent a promising platform for theranostic applications.

Oxidation and ubiquitination in neurodegeneration

It is widely accepted that protein oxidation is involved in a variety of diseases, including neurodegenerative diseases. Especially during aging, a reduction in anti-oxidant defence mechanisms leads to an increased formation of free radical oxygen species and consequently results in a damage of proteins, including mitochondrial and synaptic ones. Even those proteins involved in repair and protein clearance via the ubiquitin proteasome and lysosomal system are subject to damage and show a reduced function. Here, we will discuss a variety of mechanisms and provide examples where cognition is affected and where repair mechanisms are no longer sufficient to compensate for a dysfunction of damaged proteins or even may become toxic. Next to physiological deficits, an accumulation of deficient proteins in aggresomes may occur and result in a formation of pathological hallmark structures typical for aging and disease. A major challenge is how to prevent aberrant oxidation, given that oxidation plays an essential role in aging and neurodegenerative diseases. Particularly interesting are the possibilities to reduce the formation of radical oxygen species leading to a dysfunction of protein repair and protein clearance, or to a formation of toxic byproducts accelerating neurodegeneration.

Measurement of Nitric Oxide and Reactive Oxygen Species in the Vascular Wall

Vascular generation of nitric oxide (NO) plays an important role in the regulation of blood flow, and is counterbalanced by the formation of radical oxygen species (ROS). Thus, an imbalance in vascular NO and ROS production contributes to endothelial dysfunction, which is associated with cardiovascular disease. Here we review the main and commonly used methods that have been applied to determine vascular NO and ROS. Only NO microsensors, electron spin resonance (ESR), and NO sensitive fluorescent probes allow real time measurement of NO levels in cell suspensions, cell cultures, and isolated vascular segments in vitro, and of these techniques only NO microsensors have so far been developed for real time detection of NO in vivo. ROS formation has been detected in cell cultures by lucigenin- enhanced fluorescence, fluorescent probes e.g. 2',7'-dichlorodihydrofluorescein and dihydroethidium, by use of ESR, and also by electrochemical detection. The limitations of the electrochemical microsensors include interference from other substances, physical force on the sensors, and influence of temperature and changes in pH that may lead to artifactual changes in current. Therefore, specificity testing and calibration are pivotal, and in case of ROS, application of more than one technique is recommendable. Technical advances have allowed simultaneous detection of both NO and superoxide anion by use of electrochemical microsensors. Miniaturizing the sensors may also allow incorporation of those in lab-on- a-chip and may lead to real time measurements of NO and ROS in the coronary circulation in situ, and hence provide direct evaluation of endothelial and vascular function in cardiovascular disease.

Crystal structure of the multicopper oxidase from the pathogenic bacterium Campylobacter jejuniCGUG11284: characterization of a metallo-oxidase

Multicopper oxidases are a multi-domain family of enzymes that are able to couple oxidation of substrates with reduction of dioxygen to water. These enzymes are capable of oxidizing a vast range of substrates, varying from aromatic to inorganic compounds such as metals. This metallo-oxidase activity observed in several members of this family has been linked to mechanisms of homeostasis in different organisms. Recently, a periplasmic multicopper oxidase, encoded by Campylobacter jejuni, has been characterised and associated with copper homeostasis and with the protection against oxidative stress as it may scavenge metallic ions into their less toxic form and also inhibit the formation of radical oxygen species. In order to contribute to the understanding of its functional role, the crystal structure of the recombinant McoC (Campylobacter jejuni CGUG11284) has been determined at 1.95 Å resolution and its structural and biochemical characterizations undertaken. The results obtained indicate that McoC has the characteristic fold of a laccase having, besides the catalytic centres, another putative binding site for metals. Indeed, its biochemical and enzymatic characterization shows that McoC is essentially a metallo-oxidase, showing low enzymatic efficiency towards phenolic substrates.

The L-Arginine–Asymmetric Dimethylarginine Ratio Is Strongly Related to the Severity of Chronic Heart Failure. No Effects of Exercise Training

Background The aim of this study was to relate levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthase, L-arginine, the substrate for NO generation, and radical oxygen species (ROS) formation to severity of chronic heart failure. The effect of 4 months’ group-based exercise training was further investigated. Method and Results Eighty patients, aged 45-85 years with New York Heart Association (NYHA) functional class II-IIIb, all on optimal medical treatment, were included. A 6-minute walking test and a bicycle exercise test were performed, and fasting blood samples were collected for determination of N-terminal pro–brain natriuretic peptide (NT-proBNP), L-arginine, ADMA, and ROS generation in circulating leukocytes. ADMA levels were significantly higher in patients in NYHA functional class III versus II ( P = .024), and the L-arginine–ADMA ratio was significantly lower ( P = .005). After adjustment for covariates, L-arginine–ADMA ratio was associated with 6-minute walking distance ( P = .004), exercise capacity ( P = .026), and inversely with NT-proBNP ( P = .015). Stimulated levels of peroxynitrite on monocytes were inversely related to left ventricular ejection fraction ( P = .005). No effect of 4 weeks’ exercise training on the measured variables was obtained. Conclusions The strong relationship seen between L-arginine–ADMA ratio, ROS formation in leukocytes, and severity of chronic heart failure contributes to increased knowledge of endothelial dysfunction related to the NO pathway in such patients.

Cell Envelope Perturbation Induces Oxidative Stress and Changes in Iron Homeostasis inVibrio cholerae

The Vibrio cholerae type II secretion (T2S) machinery is a multiprotein complex that spans the cell envelope. When the T2S system is inactivated, cholera toxin and other exoproteins accumulate in the periplasmic compartment. Additionally, loss of secretion via the T2S system leads to a reduced growth rate, compromised outer membrane integrity, and induction of the extracytoplasmic stress factor RpoE (A. E. Sikora, S. R. Lybarger, and M. Sandkvist, J. Bacteriol. 189:8484-8495, 2007). In this study, gene expression profiling reveals that inactivation of the T2S system alters the expression of genes encoding cell envelope components and proteins involved in central metabolism, chemotaxis, motility, oxidative stress, and iron storage and acquisition. Consistent with the gene expression data, molecular and biochemical analyses indicate that the T2S mutants suffer from internal oxidative stress and increased levels of intracellular ferrous iron. By using a tolA mutant of V. cholerae that shares a similar compromised membrane phenotype but maintains a functional T2S machinery, we show that the formation of radical oxygen species, induction of oxidative stress, and changes in iron physiology are likely general responses to cell envelope damage and are not unique to T2S mutants. Finally, we demonstrate that disruption of the V. cholerae cell envelope by chemical treatment with polymyxin B similarly results in induction of the RpoE-mediated stress response, increased sensitivity to oxidants, and a change in iron metabolism. We propose that many types of extracytoplasmic stresses, caused either by genetic alterations of outer membrane constituents or by chemical or physical damage to the cell envelope, induce common signaling pathways that ultimately lead to internal oxidative stress and misregulation of iron homeostasis.

Green tea extract reduces induction of p53 and apoptosis in UVB‐irradiated human skin independent of transcriptional controls

Ultraviolet (UV) irradiation plays a pivotal role in human skin carcinongenesis. Preclinically, systemically and topically applied green tea extract (GTE) has shown reduction of UV-induced (i) erythema, (ii) DNA damage, (iii) formation of radical oxygen species and (iv) downregulation of numerous factors related to apoptosis, inflammation, differentiation and carcinogenesis. In humans, topical GTE has so far only been tested in limited studies, with usually very high GTE concentrations and over short periods of time. Both chemical stability of GTE and staining properties of highly concentrated green tea polyphenols limit the usability of highly concentrated green tea extracts in cosmetic products. The present study tested the utility of stabilized low-dose GTE as photochemopreventive agents under everyday conditions. We irradiated with up to 100 mJ/cm(2) of UVB light skin patches which were pretreated with either OM24-containing lotion or a placebo lotion. Biopsies were taken from both irradiated and un-irradiated skin for both immunohistochemistry and DNA microarray analysis. We found that while OM24 treatment did not significantly affect UV-induced erythema and thymidine dimer formation, OM24 treatment significantly reduced UV-induced p53 expression in keratinocytes. We also found that OM24 treatment significantly reduced the number of apoptotic keratinocytes (sunburn cells and TUNEL-positive cells). Carefully controlled DNA microarray analyses showed that OM24 treatment does not induce off-target changes in gene expression, reducing the likelihood of unwanted side-effects. Topical GTE (OM24) reduces UVB-mediated epithelial damage already at low, cosmetically usable concentrations, without tachyphylaxis over 5 weeks, suggesting GTE as suitable everyday photochemopreventive agents.

In-vitro cell confluency affects primary human dermal fibroblast sensitivity to low concentrations of t-butylhydroperoxide

Introduction: Mitochondria play a central role in ATP production, radical oxygen species (ROS) generation, calcium signaling and apoptosis. Oxidative stress derived from mitochondria is associated with intrauterine growth restriction (IUGR), cardiovascular disease, cancer and aging. The molecular link between oxidative stress and these conditions is, however, poorly understood. Interestingly, elevated levels of intracellular S-adenosylhomocysteine (SAH), a potent inhibitor of most cellular methyltransferases, is also associated with IUGR, cardiovascular disease, cancer and aging. The molecular mechanism underlying these associations is thought to be reduced methylation capacity, leading to alterations in gene expression, cell differentiation, chromatin conformation and cell phenotype. At present, accumulation of intracellular SAH is believed to be due to nutritional deficiencies or genetic polymorphisms in the folate pathway. We now suggest that oxidative stress to mitochondria may increase intracellular SAH. Accumulation of intracellular SAH following oxidative stress to mitochondria may be an important link between oxidative stress and IUGR, cardiovascular disease, cancer and aging. In order to test our hypothesis, we have begun defining sub-lethal concentrations of t-butylhydroperoxide (t-buOOH), a compound that selectively induces ROS formation in mitochondria. The second step will be to measure levels of SAH and homocysteine in treated and non-treated living cells using high perfomance liquid chromatography. Methods and Materials: Stock cultures of primary human dermal fibroblasts were grown at 37°C in 100-mm tissue culture dishes in DMEM medium supplemented with 10% bovine calf serum and 1% streptomycin. Experimental cultures (40,000 cells per well) were plated in 35-mm tissue culture dishes and allowed to grow for 24 hours. The medium was then replaced with medium containing concentrations of 1ul, 10ul or 50uM t-buOOH. Light microscopy was used to evaluate cell apoptosis, characterized by cell shrinkage and detachment from the tissue culture dish, every 12 hours for 3 days. Results: After 24 hours, experimental cell cultures exposed to 50 uM t-buOOH were uniformly killed. Experimental cultures exposed to both 10 and 1 uM t-buOOH, however, displayed apoptosis only in the periphery of the tissue culture dishes. Careful observation of control cell culture dishes revealed that after 24 hours, cell confluency was 100% centrally, while only 50% in the periphery. These findings suggest that in-vitro cell confluency affects human dermal fibroblast sensitivity to low concentrations of t-butylhydroperoxide. Discussion: In order to test our hypothesis that oxidative stress to mitochondria increases intracellular SAH, we first need to define sub-lethal concentrations of t-buOOH, a compound that selectively induces ROS formation in mitochondria. We assumed that high concentrations of t-buOOH (50 uM) would induce apoptosis of all the cells in an experimental tissue culture dish. Exposure of primary human dermal fibroblasts to 50 uM did kill all of the observed cells. We also assumed that low concentrations of t-buOOH (1 and 10 uM) might not kill any of the cells in the tissue culture dishes. We observed, however, that low concentrations of t-buOOH induced apoptosis of partially confluent peripheral cells, but not of completely confluent central cells. Therefore, in-vitro cell confluency appears to affect human dermal fibroblast sensitivity to low concentrations of t-butylhydroperoxide. Future experiments will use cell cultures that have been allowed to grow to uniform, 100% confluency before being exposed to t-buOOH test concentrations.

Oxidative stress induces actin-cytoskeletal and tight-junctional alterations in hepatocytes by a Ca 2+-dependent, PKC-mediated mechanism: Protective effect of PKA

Oxidative stress elevates Ca 2+ and, presumably, activates Ca 2+-dependent PKCs. We analyzed the participation of Ca 2+-dependent PKCs in actin disorganization and tight-junctional impairment induced by the pro-oxidant tert-butylhydroperoxide ( tBOOH) in isolated rat hepatocyte couplets. tBOOH (100 μM) augmented radical oxygen species (ROS), as indicated by increased lipid peroxidation (+217%, p < 0.05) and intracellular production of 2′,7′-dichlorofluorescein (+36%, p < 0.05). Cytosolic Ca 2+ and PKCα translocation to membrane, an indicator of PKCα activation, were also elevated by tBOOH (+100 and +79%, respectively, p < 0.05). tBOOH increased the number of couplets displaying membrane blebs (+278%, p < 0.001) and caused redistribution of F-actin. tBOOH induced tight-junctional impairment, as indicated by a reduction in the percentage of couplets retaining presecreted cholyllysylfluorescein in their canalicular vacuoles (−54%, p < 0.001). tBOOH induced redistribution of the tight-junctional-associated protein ZO-1. All these events were prevented by the panspecific PKC inhibitors H7 and staurosporine, the Ca 2+-dependent PKC inhibitor Gö6976, the intracellular Ca 2+ chelator BAPTA/AM, and the PKA activator dibutyryl-cyclic AMP. Furthermore, PKC inhibition and PKA activation not only prevented but also fully reversed tBOOH-induced blebbing. Conversely, tBOOH-induced ROS formation and Ca 2+ elevation remained unchanged. We conclude that ROS induce hepatocellular actin-cytoskeleton rearrangement and tight-junctional impairment by a PKC-mediated, Ca 2+-dependent mechanism, which is counteracted by PKA.

Endogenous Adrenomedullin Protects Against Vascular Response to Injury in Mice

In our previous study, adrenomedullin (AM) overexpression could limit the arterial intimal hyperplasia induced by cuff injury in rats. However, it remains to be elucidated whether endogenous AM plays a role against vascular injury. We used the AM knockout mice to investigate the effect of endogenous AM. Compared with wild-type (AM+/+) mice, heterozygous AM knockout (AM+/-) mice had the increased intimal thickening of the cuff-injured femoral artery, concomitantly with lesser AM staining. In AM+/- mice, cuff placement increased both the production of superoxide anions (O2-) measured by coelentarazine chemiluminescence and the immunostaining of p67phox and gp91phox, subunits of NAD(P)H oxidase in the adventitia, associated with the increment of CD45-positive leukocytes, suggesting that the stimulated formation of radical oxygen species accompanied chronic adventitial inflammation. Not only the AM gene transfection but also the treatment of NAD(P)H oxidase inhibitor apocynin and membrane-permeable superoxide dismutase mimetic tempol could limit cuff-induced intimal hyperplasia in AM+/- mice, associated with the inhibition of O2- formation in cuff-injured artery. The overproduction of oxidative stress induced by the increased NAD(P)H oxidase activity might be involved in cuff-injured arterial intimal hyperplasia in AM+/- mice. Thus, it is suggested that endogenous AM possesses a protective action against the vascular response to injury, possibly through the inhibition of oxidative stress production.

Formation of radical oxygen species on hydroxyapatite

Hydroxyapatite of approximately stoichiometric composition ( Ca P molar ratio 1.65) evacuated at 600°C and exposed to O 2 at room temperature produces ESR spectra with g xx = 2.0013, g yy = 2.0102 and g zz = 2.0160, providing evidence for the formation of O − 2. Although the ESR signal attributed to Fs + centers is observable on both nonstoichiometric apatite ( Ca P molar ratio 1.61) and the stoichiometric form, no change in the ESR signal of the former sample takes place after adsorption of oxygen at room temperature. The formation of O − 2 suggests presence of O 2− of low coordination in the stoichiometric form.

Production of free radicals arising from the surface activity of minerals and oxygen. Part I. Iron mine ores.

The excess incidence of lung cancers observed in many metal mines probably is not only correlated with radioactivity but also with the inhaled dusts. In an attempt to determine a possible mechanism of carcinogenicity related to the surface activity of dusts, using the spin-trapping agent and ESR spectroscopy, one can demonstrate that some mineral dusts from iron ore mines are very active in an oxidative process in aqueous medium, implying the formation of radical oxygen species on reducing surface sites of the solid. This reducing surface activity of the dusts depends on the presence of Fe2+ ion in the lattice and on the process of activation and passivation of the surface sites. The more simple process of activation is the dissolution of the oxidized coating on the particle surface. Among the oxides, oxyhydroxides, carbonates, and silicates, the magnesium-iron phyllosilicates (chlorite, biotite, berthierine) appear the most active. The siderite FeCO3 is also active, but the iron oxides and oxyhydroxides are generally nonactive.

Investigations of catalytically active surface compounds: XVII. Influence of size and structure of vanadium oxide clusters on selectivity in the oxidation of n-butene

n-Butene oxidation on vanadium oxide monolayer catalysts (supported on Aerosil-200) was investigated in the temperature range from 633 to 693 K using two types of active vanadium oxide components differing with respect to the size of the clusters and the coordination of the vanadium ions. Coordination is characterized by uv-vis spectroscopy. The degree of reduction of vanadium in a state close to reaction conditions was determined by titration of suitably pretreated samples. In the conversion range between 7 and 95%, selectivities for butadiene, furan, maleic anhydride, acetaldehyde, CO, and CO 2 were determined, initial selectivities S 0 being estimated by extrapolation to zero conversion. A formal reaction scheme including direct formation of products without desorption and readsorption of preceding intermediates is proposed. From comparison of the values of S 0 and κ (ratio of rate constants for formation and consumption of primary products) characteristic features of the different catalytic behavior of the two active surface phases have been derived. Selectivity is mainly influenced by the amount and the nature of oxygen available in the cluster, by the bond strength of oxygen in the cluster unit, and by the probability of formation of radical oxygen species.