Iron-catalyzed Decomposition Research Articles

ChemInform Abstract: Homogeneous Catalytic Processes Monitored by Combined in situ ATR‐IR, UV‐Vis, and Raman Spectroscopy

AbstractReview: 57 refs.

Homogeneous Catalytic Processes Monitored by Combined in Situ ATR-IR, UV–Vis, and Raman Spectroscopy

The benefit of coupling in situ spectroscopic methods (attentuated total reflectance-infrared spectroscopy (ATR-IR), Raman, and UV–vis) for the real-time monitoring of homogeneously catalyzed reactions is exemplarily demonstrated on selected examples of use. In this context, the different mode of catalyst action in reduction reactions of imides and amides with phenylsilanes will be discussed. In the iron-catalyzed decomposition of formic acid, different intermediate iron complexes were identified and the inhibiting effect of chloride onto active iron complex formation could be elucidated. Furthermore, it could be shown that in a Lewis acid catalyzed cyclocondensation reaction, the reactant activation proceeds differently with AlCl3 and TiCl4. For the described in situ spectroscopic studies, a versatile setup was used which allows the simultaneous registration of ATR-IR, UV–vis, and Raman spectra in small volumes of solution at different reaction-determined conditions using fiber-optic probes for the each spectroscopy.

FeS-Induced Radical Formation and Its Effect on Plasmid DNA

Plasmid DNA was incubated at 25°C with aqueous solutions of dissolved Fe(II), S(-II), and nanoparticulate FeS with a mackinawite structure, FeSm. At ≥0.1 mM total dissolved Fe(II) and S(-II), an increase in the proportion of the relaxed plasmid DNA occurs, through scission of the DNA backbone. In solutions where FeSm was precipitated, nanoparticulate FeSm binds to the DNA molecules. In solutions with concentrations below the FeSm solubility product, nicking of supercoiled pDNA occurs. Plasmid DNA appears to be a sensitive proxy for radical reactions. The reactant is proposed to be a sulfur-based radical produced from the iron-catalyzed decomposition of bisulfide, in a manner analogous to the Fenton reaction. This is further supported by experiments that suggest that sulfide free radicals are produced during the photolysis of aqueous solutions of polysulfides. Supercoiling of DNA affects nearly all DNA–protein transactions so the observation of relaxation of supercoiled forms through reaction with FeS solutions has direct implications to biochemistry. The results of this experimentation suggest that genotoxicity in FeS-rich systems is a further contributory factor to the limited survival of organisms in sulfidic environments. Mutations resulting from the interactions of organisms and mobile elements, such as plasmids, in sediments will also be affected in sulfide-rich environments.

Formation of mononuclear nitrosyl intermediates during hydrolysis of [Na2[Fe2(μ-S2O3)2(NO)4]·4H2O, a donor of nitrogen monoxide

One of the effects of endogenous NO is the formation of dinitrosyl iron complexes (DNICs), which, along with nitrosothiols, have been identified in all life forms, i.e., in the cells of bacteria, plants, and mammals [1]. Nitrosyl nonheme iron complexes have been identified by EPR as products of interaction of NO with some iron‐sulfur proteins and other iron-containing proteins [2‐5]. DNICs are intermediates in the iron-catalyzed decomposition and formation of S- nitrosothiols [6] and are considered as NO reservoirs and transporters in vivo. These results initiated the development of methods of synthesis and study of the physical and chemical properties of synthetic DNIC analogues [7] with the aim of their practical use as NO donors in medicine and biology [8, 9]. In the present paper, we report the results of the mass spectral and electrochemical studies of the products of hydrolysis of the tetranitrosyl iron thiosulfate complex Na 2 [Fe 2 ( µ -S 2 O 3 ) 2 (NO) 4 )] · 4 H 2 O (TNIC) in aqueous solutions. Study of the antimetastatic effect of the TNIC on three experimental models—melanoma B16, LL carcinoma, and AKATOL—showed that the complex inhibits metastatic growth. The combined administration of a low ineffective dose of the TNIC with cisplatin (or adriablastin) in leukemia P 388‐bearing mice leads to 100% survival among the laboratory animals [10]. Studying the TNIC decomposition products in solutions and determining the structure and properties of intermediates formed during hydrolysis are important for an understanding of molecular genetic mechanisms of action of exogenous NO donors of this class.

The synthesis of structured Pd/C hydrogenation catalysts by the chemical vapor deposition of Pd(allyl)Cp onto functionalized carbon nanotubes anchored to vapor grown carbon microfibers

Vapor grown carbon fibers (VGCF) were prepared by the iron-catalyzed decomposition of methane. The as-grown microfibers were treated by HNO 3, and iron nanoparticles were deposited onto the fiber surface by impregnation. Carbon nanotubes (CNT) were grown homogeneously as branches on the microfiber surface by tuning the process parameters of the methane decomposition. A composite carbon nanotube–carbon microfiber (CNT–VGCF) system was thus obtained and used as support for palladium nanoparticles. Oxygen-containing functional groups were introduced into the CNT–VGCF system by plasma treatment in a fluidized-bed reactor. The Pd/C catalyst was prepared by chemical vapor deposition on the CNT–VGCF support using Pd(allyl)Cp as a precursor (MOCVD) in a fixed-bed reactor. The effects of the surface treatment and the deposition of palladium were investigated by X-ray photoelectron spectroscopy (XPS). Only traces of palladium were detected after deposition on as-grown fibers, whereas a significantly higher concentration was found on plasma-treated fibers. The catalytic activity of the Pd/C catalyst was evaluated by the hydrogenation of cyclooctene in a fixed-bed microreactor under plug-flow conditions. The CNT–VGCF system was found to be a suitable structured support for Pd nanoparticles.

Iron-catalyzed reaction products of α-tocopherol with 1-palmitoyl-2-linoleoyl-3- sn-phosphatidylcholine (13 S)-hydroperoxide

α-Tocopherol was reacted with 1-palmitoyl-2-[(9 Z,11 E)-( S)-13-hydroperoxy-9,11-octadecadienoyl]-3- sn-phosphatidylcholine (13-PLPC-OOH) in the presence of a lipid-soluble iron chelate, Fe(III) acetylacetonate, in methanol at 37 °C. The reaction product was isolated and identified as a mixture of 1-palmitoyl-2-[(10 E)-(12 S,13 S)-9-(8a-dioxy-α-tocopherone)-12,13-epoxy-10-octadecenoyl]-3- sn-phosphatidylcholine and 1-palmitoyl-2-[(9 Z)-(12 S,13 S)-11-(8a-dioxy-α-tocopherone)-12,13-epoxy-9-octadecenoyl]-3- sn-phosphatidylcholine (TOO-epoxyPLPC), in which the 12,13-epoxyperoxyl radicals derived from 13-PLPC-OOH attacked the 8a-position of the α-tocopheroxyl radical. The iron and ascorbate-catalyzed reaction of 13-PLPC-OOH with α-tocopherol in phosphatidylcholine (PC) liposomes was assessed by measuring the reaction products of α-tocopherol. When 13-PLPC-OOH and α-tocopherol were added in saturated dimyristoyl-PC liposomes, the products were TOO-epoxyPLPC, α-tocopherylquinone, and epoxy-α-tocopherylquinones. In 1-palmitoyl-2-linoleoyl-PC (PLPC) liposomes, α-tocopherol could react with both the 13-PLPC-OOH derived 12,13-epoxyperoxyl radicals and the PLPC-derived peroxyl radicals and formed the addition products together with α-tocopherylquinone and epoxy-α-tocopherylquinones. Therefore, the iron-catalyzed decomposition of phospholipid hydroperoxides primarily produces epoxyperoxyl radicals, which react with the 8a-carbon centered radical of α-tocopherol in liposomal systems.

DNA oxidative damage during differentiation of HL-60 human promyelocytic leukemia cells.

DNA oxidative damage was measured in human promyelocytic leukemia HL-60 cells, in the same cells committed to granulocytic differentiation with dimethyl sulfoxide (DMSO) or all-trans-retinoic acid (RA) and in mature human peripheral granulocytes (HPG). DNA damage was evaluated as single strand breaks and 8-OHdG adducts, measured by single cell electrophoresis or by monoclonal antibodies, respectively. The basal levels of either marker of DNA damage were higher in undifferentiated HL-60 cells than in HPG and DMSO- or RA-differentiated cells. Treatment with H(2)O(2) increased 8-OHdG formation in all cells, but the levels of DNA damage remained higher in undifferentiated cells as compared to the differentiated ones. Three lines of evidence suggested that the higher levels of DNA damage observed in undifferentiated cells were at least in part attributable to a reduced detoxification of reactive oxygen species (ROS). First, undifferentiated cells were shown to accumulate higher levels of dichlorodihydrofluorescein-detectable ROS than HPG and DMSO- or RA-differentiated cells. Second, undifferentiated HL-60 cells were characterized by reduced levels of GSH and lower GSH/GSSG ratios as compared to the differentiated cells. Third, pretreatment of undifferentiated HL-60 cells with antioxidants such as alpha-tocopherol or beta-carotene suppressed the elevation of ROS and the formation of 8-OHdG induced by H(2)O(2). Further evidence for the importance of the oxidant/antioxidant balance was obtained by modulating the iron-catalyzed decomposition of H(2)O(2) to hydroxyl radicals in undifferentiated HL-60 cells. In fact, pretreatment with FeSO(4) increased the formation of 8-OHdG induced by H(2)O(2), whereas pretreatment with the iron chelator deferoxamine produced the opposite effect. These results illustrate correlations between the oxidant/antioxidant balance and DNA damage and suggest that the capability of a cell population to withstand oxidative stress and DNA damage may depend on its degree of differentiation.

The role of reactive oxygen species in triggering proliferation and IL-2 secretion in T cells

This paper examines the hypothesis that reactive oxygen species (ROS) play an important role as second messengers in T cell activation. Activation of T cells with phorbol ester in combination with either calcium ionophore, or anti-CD3 antibody results in a large rapid flux of ROS activity. In contrast, co-stimulation with CD28 does not enhance ROS activity. The ROS signal was sensitive to ascorbic acid, desferrioxamine and dimethyl sulfoxide, suggesting that the major active species being generated was the hydroxyl radical, probably by iron-catalyzed decomposition of hydrogen peroxide. The generation of ROS in T cells was regulated by an accessory population within the peripheral blood. An anti-CD2 antibody induced a strong ROS flux, suggesting that the CD2/LFA-3 interaction may be important in this regulation. T cell activation was inhibited by the same panel of anti-oxidants as ROS generation, but much higher concentrations were required for inhibition of proliferation and IL-2 release than those required to block ROS generation. These data imply that ROS are not obligate second messengers for initiation of T cell activation. The results are compatible, however, with a role for activation-dependent T cell ROS generation in modulating the overall T cell response via autocrine and paracrine signalling pathways.

Electron spin resonance evidence of the generation of superoxide anion, hydroxyl radical and singlet oxygen during the photohemolysis of human erythrocytes with bacteriochlorin a.

Photodynamic therapy with bacteriochlorin a (BCA) as sensitizer induces damage to red blood cells in vivo. To assess the extent of the contributuion of reactive oxygen species (ROS) and to determine a possible reaction mechanism, competition experiments with assorted ROS quenching or/and enhancing agents were performed in human erythrocytes as model system and in phosphate buffer. In the erythrocyte experiments, a 2% suspension was incubated with BCA for 1 h, washed with phosphate-buffered saline, resuspended and subsequently illuminated with a diode laser using a fluence rate of 2.65 mW/cm2. Potassium leakage and hemolysis were light and BCA dose dependent. Adding tryptophan (3.3 mM), azide (1 mM) or histidine (10 mM) to the erythrocyte suspension before illumination delayed the onset of K-leakage and hemolysis suggesting a type II mechanism. The D2O did not affect K-leakage nor photohemolysis. Adding mannitol (13.3 mM) or glycerol (300 nM) also caused a delay in the onset of K-leakage and hemolysis, suggesting the involvement of radicals. In phosphate buffer experiments, it was shown using electron spin resonance (ESR) associated with spin-trapping techniques that BCA is able to generate O2-. and OH. radicals without production of aqueous electron. Visible or UV irradiation of the dye in the presence of the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) gave an ESR spectrum characteristic of the DMPO-hydroxyl radical spin adduct DMPO-OH. Addition of ethanol or sodium formate produced supplementary hyperfine splittings due to the respective CH3CHOH. and CO2-. radical adducts, indicating the presence of free OH.. Production of DMPO-OH was partly inhibited by superoxide dismutase (SOD), catalase and desferrioxamine, suggesting that the iron-catalyzed decomposition of H2O2 was partly involved in the formation of one part of the observed OH.. The complementary inhibition of DMPO-OH production by azide and 9,10-anthracenedipropionic acid (ADPA) was consistent with 1O2 production by BCA followed by reaction of 1O2 with DMPO and decay of the intermediate complex to form DMPO-OH and free OH.. All our results seem to indicate that BCA is a 50%/50% type 1/type 2 sensitizer in buffered aqueous solutions and confirmed that the dye-induced hemolysis of erythrocytes was cell caused by a mixed type 1/type 2 mechanism.

Free Radical Reactions in Aqueous Solutions: Examples from Advanced Oxidation Processes for Wastewater from the Chemistry in Airborne Water Droplets

Inorganic chemistry involving free radicals in aqueous solutions can be important in environmental processes. A common free radical reaction in aqueous solution is electron transfer, especially to the hydroxyl radical and to ozone. Hydrogen peroxide and free radicals related to it act as weak acids, so both their neutral and deprotonated forms must be considered in reactions. In Advanced Oxidation Processes, the hydroxyl radical concentration in water is greatly increased by reactions involving ozone and/or ultraviolet light. Irradiation of solid titanium dioxide can also be used to generate the radicals. The hydroxyl radicals are used in the Processes to initiate the oxidation of dissolved organic pollutants. Free radical reactions also play an important role in the chemistry of water droplets suspended in air in clouds and fogs. The radicals arise indirectly from the photoionization of dissolved organic compounds such as aldehydes and from the iron-catalyzed decomposition of dissolved hydrogen peroxide. They oxidize dissolved sulfur dioxide and certain organic compounds.

Equilibrium shape equation and possible shapes of carbon nanotubes.

The elastic free energy of carbon nanotubes grown by iron-catalyzed decomposition of acetylene is introduced to describe the possible tubular shapes. The equilibrium shape equation can be obtained by the first variation of the elastic free energy of the slightly distorted tube. The model is consistent with both stable and metastable shapes observed in our experiments. The results are due to the fluctuation of growth conditions, such as the pressure, temperature, and composition of the vapor. \textcopyright{} 1996 The American Physical Society.

Antioxidant Action of Neuromelanin: The Mechanism of Inhibitory Effect on Lipid Peroxidation

Iron and lipid peroxidation are believed to be involved in the degeneration of pigmented neurons in Parkinson′s disease. Melanin-iron interaction is thought to play a role in iron accumulation and reactivity. The purpose of this study was to examine antioxidant properties of isolated natural and synthetic neuromelanin. Effect of neuromelanin from substantia nigra and its synthetic model, dopamine melanin, on Lipid peroxidation, induced by ferrous ions and free-radical initiators, has been studied in methyl linoleate aqueous dispersions, 2,2′-azobis(amidinopropane)dihydrochloride and 2,2′-azobis(2,4-dimethyl-valeronitrile) were used as water-soluble and lipid-soluble radical initiator, respectively. Rate of oxidation was followed quantitatively by measuring oxygen uptake and accumulation of lipid hydroperoxides. Melanin had a distinct protective effect on lipid peroxidation induced by ferrous ions or water-soluble free-radical initiator but was relatively inefficient when peroxidation was initiated with lipid-soluble compound. It also inhibited iron-catalyzed decomposition of methyl linoleate hydroperoxides in the presence of ascorbate. Extent of the inhibition depended on the ratio of melanin to iron. Taken together, these results provide strong support for the idea that neuromelanin of pigmented neurons can act as a natural antioxidant by sequestering redox-active metal ions.

Lethal damage to endothelial cells by oxidized low density lipoprotein: role of selenoperoxidases in cytoprotection against lipid hydroperoxide- and iron-mediated reactions.

Oxidized low density lipoprotein (LDLox) is believed to be an important contributor to endothelial cytodamage and atherogenesis. The purpose of this study was to examine the role of glutathione (GSH) and GSH-dependent selenoperoxidases in cytoprotection against the damaging effects of LDLox. When irradiated in the presence of a phthalocyanine sensitizing dye, human LDL accumulated chromatographically detectable and iodometrically measurable lipid hydroperoxides (LOOHs). Photogenerated LDLox caused lethal damage to bovine aortic endothelial (BAE) cells in vitro, as determined by lactate dehydrogenase release and inhibition of thiazolyl blue reduction. When depleted of GSH by buthionine sulfoximine treatment, BAE cells became more sensitive to LDLox. Cells grown in 2% serum/DME-HAM's F-12 medium without added selenium [Se(-) cells] exhibited far lower GSH-peroxidase and phospholipid hydroperoxide GSH-peroxidase activities than selenium-supplemented controls [Se(+) cells], and were much more sensitive to oxidative injury induced by t-butyl hydroperoxide, liposomal cholesterol hydroperoxides, and LDLox. Preincubation of LDLox with GSH and Ebselen (a selenoperoxidase mimetic) resulted in a dramatic reduction in both LOOH content and cytotoxicity. Moreover, treating Se(-) cells themselves with Ebselen substantially restored their resistance to LDLox-induced damage. LDLox toxicity to Se(-) cells was strongly inhibited by desferrioxamine and stimulated by ferric-8-hydroxyquinoline (a lipophilic chelate), indicating that iron is an active participant in oxidative damage. These results demonstrate that the GSH-dependent selenoperoxidase(s) play(s) an important role in cellular defense against oxidized low density lipoprotein, presumably by detoxifying lipid hydroperoxides and thereby preventing their iron-catalyzed decomposition to damaging free radical intermediates.

The effect of melanin on iron associated decomposition of hydrogen peroxide

The effects of melanin on the iron-catalyzed decomposition of hydrogen peroxide to hydroxyl radicals and hydroxyl ions have been studied using electron spin resonance, spin trapping and visible light spectrophotometry. Melanin altered these reactions by several different mechanisms and consequently, depending on conditions, can significantly increase or decrease the yield of reactive products, including hydroxyl radicals. For low concentrations of ferrous ions, melanin decreased the yield of hydroxyl radicals due to binding of ferrous ions by melanin; ferrous ions bound to melanin did not decompose H 2O 2 efficiently. Melanins increased the rate of hydroxyl radical production if the predominant form of iron was ferric, dur to the ability of melanin to reduce ferric to ferrous iron. Hydroxyl radical production in the presence of a strong chelator (e.g. EDTA) and melanin was greater than in the presence of a weak chelator (e.g. ADP) and melanin. Melanin also increased the rate of destruction of the DMPO-OH adduct.

Interaction between oxygen radicals and gastric mucin.

The gastrointestinal epithelium is continuously exposed to reactive oxygen metabolites that are generated within the lumen. In spite of this exposure, the healthy epithelium appears unaffected, suggesting efficient mechanisms for protection against these potentially cytotoxic oxidants. The objective of this study is to characterize the interaction between purified gastric mucin and hydroxyl radicals generated from the interaction between ferric iron and ascorbic acid. We found that both native and pronase-treated mucin effectively scavenged hydroxyl radical and that the scavenging properties were not significantly different. The effective concentration of mucin required for a 50% reduction in malondialdehyde production was approximately 10 mg/ml for both native and pronase-treated mucin. In addition, the iron-ascorbic system produced a dramatic decrease (greater than 50%) in the specific viscosity of mucin that was inhibited by catalase, deferoxamine, and mannitol. Superoxide dismutase had no effect. These data suggest that hydroxyl radicals derived from the iron-catalyzed decomposition of hydrogen peroxide are responsible for the depolymerization of native mucin. We propose that mucin may provide protection to the surface epithelium of the gastrointestinal tract by scavenging oxidants produced within the lumen; however, it does so at the expense of its viscoelastic properties.

Smectite clays in Mars soil: evidence for their presence and role in Viking biology experimental results.

Various chemical, physical and geological observations indicate that smectite clays are probably the major components of the Martian soil. Satisfactory ground-based chemical simulation of the Viking biology experimental results was obtained with the smectite clays nontronite and montmorillonite when they contained iron and hydrogen as adsorbed ions. Radioactive gas was released from the medium solution used in the Viking Labeled Release (LR) experiment when interacted with the clays, at rates and quantities similar to those measured by Viking on Mars. Heating of the active clay (mixed with soluble salts) to 160 degrees C in CO2 atmosphere reduced the decomposition activity considerably, again, as was observed on Mars. The decomposition reaction in LR experiment is postulated to be iron-catalyzed formate decomposition on the clay surface. The main features of the Viking Pyrolytic Release (PR) experiment were also simulated recently (Hubbard, 1979) which the iron clays, including a relatively low '1st peak' and significant '2nd peak'. The accumulated observations on various Martian soil properties and the results of simulation experiments, thus indicate that smectite clays are major and active components of the Martian soil. It now appears that many of the results of the Viking biology experiments can be explained on the basis of their surface activity in catalysis and adsorption.