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PubMed1997

Interaction of nitric oxide with non-haem iron sites of Escherichia coli bacterioferritin: reduction of nitric oxide to nitrous oxide and oxidation of iron(II) to iron(III).

The bacterioferritin (BFR) of Escherichia coli consists of 24 identical subunits, each containing a dinuclear metal-binding site consisting of two histidines and four carboxylic acid residues. Earlier studies showed that the characterization of iron binding to BFR could be aided by EPR analysis of iron-nitrosyl species resulting from the addition of NO to the protein [Le Brun, Cheesman, Andrews, Harrison, Guest, Moore and Thomson (1993) FEBS Lett. 323, 261-266]. We now report data from gas chromatographic head space analysis combined with EPR spectroscopy to show that NO is not an inert probe: iron(II)-BFR catalyses the reduction of NO to N2O, resulting in oxidation of iron(II) at the dinuclear centre and the subsequent detection of mononuclear iron(III). In the presence of excess reductant (sodium ascorbate), iron(II)-BFR also catalyses the reduction of NO to N2O, giving rise to three mononuclear iron-nitrosyl species which are detectable by EPR. One of these, a dinitrosyl-iron complex of S = 1/2, present at a maximum of one per subunit, is shown by EPR studies of site-directed variants of BFR not to be located at the dinuclear centre. This is consistent with a proposal that the diferric form of the centre is unstable and breaks down to form mononuclear iron species.

Bacterial Proteins↗

PubMed2005

Temperature-dependent growth of germanium oxide and silicon oxide based nanostructures, aligned silicon oxide nanowire assemblies, and silicon oxide microtubes.

We demonstrate the temperature-dependent growth of germanium oxide and silicon oxide based composite nanostructures (multiple nanojunctions of Ge nanowires and SiO(x) nanowires, Ge-filled SiO(2) nanotubes, Ge/SiO(2) coaxial nanocables, and a variety of interesting micrometer-sized structures), aligned SiO(x) nanowire assemblies, and SiO(x) microtubes. The structures were characterized by SEM, TEM, energy-dispersive X-ray spectroscopy, and electron diffraction. The combination of laser ablation of a germanium target and thermal evaoporation of silicon monoxide powders resulted in the formation of Ge and SiO(x) species in a carrier gas; the nano/micro-sized structures grow by either a Ge-catalyzed vapor-liquid-solid or a Ge-nanowire-templated vapor-solid process.

Crystallization↗

PubMed1981

[Carcinogenic activity of ethylene oxide and its reaction products 2-chloroethanol, 2-bromoethanol, ethylene glycol and diethylene glycol. I. Carcinogenicity of ethylene oxide in comparison with 1,2-propylene oxide after subcutaneous administration in mice (author's transl)].

Ethylene oxide is an important initial product for a number of organic compounds and, in addition, is used in the medical field for sterilization. The aim of our experiments was to test ethylene oxide and, as a comparative substance, 1,2-propylene oxide in respect to their cancerogenic effectiveness in animal experiments. Ethylene oxide was administered subcutaneously in three dosages (1.0; 0.3 and 0.1 mg single dosage per mouse) once per week to groups of 100 female NMRI mice respectively. In the case of 1,2-propylene oxide, four dosages were used (2.5; 1.0; 0.3 and 0.1 mg single dosage per mouse). The vehicle was tricaprylin. Administrations were carried out over a period of 95 weeks. The mean total dosage per mouse in the case of ethylene oxide amounted to 64.4; 22.7, and 7.3 mg and, in the case of propylene oxide, to 165.4; 72.8; 21.7 and 6.8 mg. Both substances induced local tumours depending upon the dosage. There were mostly fibrosarcomas. In the case of the groups treated with ethylene oxide the frequency was between 11 and 5% and in the case of the groups treated with 1,2-propylene oxide this was between 16 and 2%. The cancerogenic effect of ethylene oxide and 1,2-propylene oxide determined in animal experiments could, therefore, be confirmed statistically. On the basis of the results presented in this paper, new aspects have arisen for the medical evaluation of ethylene oxide residues in the field of manufacturing and use and in respect to the TLV.

Animals↗

PubMed1992

Chemical oxidation of N-hydroxyguanidine compounds. Release of nitric oxide, nitroxyl and possible relationship to the mechanism of biological nitric oxide generation.

N omega-Hydroxy-L-arginine was found to cause vasodilation in arginine-depleted rabbit aorta. It is, therefore, likely to be a biosynthetic intermediate in the conversion of arginine to nitric oxide in this tissue. N-Hydroxyalkylguanidine compounds, including N omega-hydroxy-L-arginine were oxidized with various oxidizing agents and examined for their ability to release nitric oxide. All oxidizing agents tested were capable of oxidizing the N-hydroxyguanidine function but only lead tetra-acetate (Pb(OAc)4) and potassium ferricyanide/hydrogen peroxide (K3FeCN6/H2O2) were capable of generating significant amounts of nitric oxide. Oxidation with K3FeCN6, lead oxide (PbO2) and silver carbonate (Ag2CO3) resulted instead in the release of nitrous oxide (N2O) presumably through the initial release of nitroxyl (HNO).

Animals↗

PubMed1998

Glyc-oxidized LDL impair endothelial function more potently than oxidized LDL: role of enhanced oxidative stress.

Hypercholesterolemia is associated with impairment of endothelial function due to increased levels of LDL. In diabetic patients, however, attenuation of endothelial function occurs even under normocholesterolemic conditions. Here we assessed whether glycation of LDL potentiates their influence on endothelial function, with particular emphasis on the oxidizability of LDL and the role of O2-. Human LDL was glycated by dialyzation for 7 days against buffer containing 200 mmol/l glucose, or sham-treated without glucose, and oxidized by incubation with Cu2+. Glycation significantly enhanced the oxidizability of LDL, as detected by diene formation and by electrophoretic mobility (27.5 mm for oxidized LDL vs. 34 mm for oxidized glycated LDL at 20 h of oxidation). Isolated rings of rabbit aorta were superfused with physiological salt solution, and isometric tension was recorded. Incubation of the aortic rings with sham-treated or with glycated LDL, not oxidized, had no influence on acetylcholine-induced, endothelium-dependent relaxation. Exposure of the aortic rings to oxidized non-glycated LDL caused a significant inhibition (30% at 1 microM acetylcholine) of the endothelium-dependent relaxation only in the presence of diethyl-dithiocarbamate (DDC), an inhibitor of the endogenous superoxide dismutase (SOD). Incubation of aortic rings with oxidized glycated LDL attenuated endothelium-dependent relaxation even in the absence of DDC (by 31% at 1 microM acetylcholine). The presence of DDC potentiated the inhibition of relaxation (65% inhibition at 1 microM acetylcholine), and co-incubation with exogenous SOD and catalase prevented the inhibition of relaxation, indicating a mediator role of O2-. Endothelium-independent relaxation induced by forskolin was unaffected by any of the lipoproteins. Using a chemiluminescence assay, significantly increased O2- production of aortic rings pretreated with oxidized glycated LDL (4101 +/- 360 counts/s) in comparison to control rings (753 +/- 81 counts/s) or arteries pretreated with oxidized non-glycated LDL (2358 +/- 169 counts/s) could be detected, suggesting that enhanced NO-inactivation by O2- could be the underlying mechanism for the stronger impairment of endothelium-dependent dilations by oxidized glycated LDL. Glycation increases the oxidizability of LDL and potentiates its endothelium-damaging influence. The likely mechanism for attenuation of endothelium-dependent dilations is increased formation of O2-, resulting in inactivation of nitric oxide. This mechanism may play an important role in diabetic patients and may contribute to disturbed organ perfusion.

Animals↗

PubMed1993

Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects.

The purpose of this study was to understand better the factors providing oxidation resistance to human low-density lipoprotein (LDL). Therefore, the susceptibility to copper-induced in vitro oxidation of LDL from vitamin E deficient patients and normal healthy subjects was studied. Surprisingly, the LDL of vitamin E deficient patients appeared less susceptible to oxidation than control LDL. Both oxidation rate and extent of oxidation, measured as diene production, were reduced when compared to control LDL. The lag time, a measure of resistance to oxidation, was not different from the lag time of LDL from healthy subjects. No relation was found between vitamin E content and resistance against oxidation. LDL from vitamin E deficient patients contained lower amounts of vitamin E, less cholesteryl esters, and increased amounts of triglycerides. Furthermore, its oleic acid content was increased and its linoleic acid content decreased. Linear regression analyses revealed that the ratio of oleic acid content to linoleic acid content was strongly correlated with the lag time, and inversely correlated with oxidation rate and extent of oxidation. Thus, LDL rich in oleic acid and poor in linoleic acid was less easily oxidized. It is concluded that the susceptibility of LDL to oxidation is determined not only by its antioxidant content, but also by other compositional factors, and more specifically by the ratio of oleic acid content to linoleic acid content.

Adult↗

PubMed2004

Edaravone, a novel radical scavenger, inhibits oxidative modification of low-density lipoprotein (LDL) and reverses oxidized LDL-mediated reduction in the expression of endothelial nitric oxide synthase.

Edaravone, a newly synthesized synthetic radical scavenger, has been identified and adopted as an anti-stroke agent. However, its mechanism and the effect of edaravone on lipoprotein oxidation are not fully understood. Therefore, whether edaravone could suppress oxidation of low-density lipoprotein (LDL) and be involved in the expression of endothelial nitric oxide synthase (eNOS) in relation to anti-atherogenesis by improving and conserving vascular circulation was investigated. We investigated the in vitro effects of edaravone on copper- and endothelial cell-mediated LDL oxidation, and the expression of eNOS in human umbilical vein endothelial cells (HUVEC) modulated by oxidized LDL. The in vivo effect of edaravone on antioxidative effect was also studied in male rats intravenously administered with edaravone. Edaravone apparently inhibited copper- and HUVEC-mediated LDL oxidation at the concentration equivalent to serum concentrations in clinical use. The intravenous administration of edaravone also enhanced serum radical-scavenging property in rats. We tested the effect of edaravone on protein and mRNA expression of eNOS in HUVEC. Edaravone enhanced eNOS expression in HUVEC, presumably because of increased stability of eNOS mRNA, and reversed eNOS expression reduced by oxidized LDL nearly to the control levels. The present study demonstrates for the first time that edaravone increases eNOS expression with the inhibition of LDL oxidation, and that edaravone can reverse oxidized LDL-mediated reduction in eNOS expression in endothelial cells. The preventive action of edaravone from ischemic disease consequence may be attributed to these eNOS up-regulation with decreased oxidation.

Animals↗

PubMed2003

Ageing of chromium(III)-bearing slag and its relation to the atmospheric oxidation of solid chromium(III)-oxide in the presence of calcium oxide.

Slag arising in ferrochromium and stainless steel production is known to contain residual levels of trivalent chromium. As the chromium is normally bound in the slag matrix in various silicate or spinel phases, and hence not easily mobilised, utilisation or controlled disposal of such slag is generally considered unproblematic. Experimental test work with a number of slag materials indicates, however, that very gradual oxidation of trivalent to hexavalent chromium does occur when the slag is exposed to atmospheric oxygen, rendering a quantifiable but small portion of chromium in this much more mobile and toxic form. Mechanisms and rates of the oxidation reaction were investigated in a number of long-term studies using both original slag materials and artificial mixes of chromium and calcium oxides. Powders of these materials, some of them rolled into balls, were left to age under different conditions for periods of up to 12 months. In the slag samples, which contained between 1 and 3 wt.% chromium, 1000-10000 microg Cr(VI) were found per gram of chromium within 6-9 months of exposure to an ambient atmosphere. The rate of the oxidation reaction decreased exponentially, and the reaction could generally be said to have ceased within 12 months. In mixtures of calcium and chromium oxides the oxidation reaction is presumed to occur at the boundaries between chromium oxide and calcium oxide phases through diffusion of oxygen along the grain boundaries and of Cr(3+) across the boundaries, resulting in the formation of calcium chromate. In the slags, where calcium and chromium oxide can form a solid solution, the oxidation is likely to occur at the exposed surface of grains containing this solution.

Atmosphere↗

PubMed2006

Enhanced oxidation of NAD(P)H by oxidants in the presence of dehydrogenases but no evidence for a superoxide-propagated chain oxidation of the bound coenzymes.

Recently we demonstrated that lactate dehydrogenase (LDH)-bound NADH is oxidized by O2, H2O2, HNO2 and peroxynitrite predominantly via a chain radical mechanism which is propagated by superoxide. Here we studied both whether other dehydrogenases also increase their coenzymes' reactivity towards these oxidants and whether a chain radical mechanism is operating. Almost all dehydrogenases increased the oxidation of their physiological coenzymes by at least one of the oxidants. The oxidation of NADH or NADPH depended both on the binding dehydrogenase and the applied oxidant and in some cases the reactions were remarkably fast. The highest rate constant (k = 370 M-1 s-1) was found for the reaction of HNO2 with NADH bound to alcohol dehydrogenase. Regardless of the applied oxidant, superoxide dismutase failed to inhibit the oxidation of protein-bound NADH and NADPH. We therefore conclude that several dehydrogenases increase the oxidation of NADH and/or NADPH by the employed set of oxidants in bimolecular reactions, but, unlike LDH, do not mediate a O2*(-) dependent chain radical mechanism.

Animals↗

PubMed1992

Oxidative inactivation of carbamoyl phosphate synthetase (ammonia). Mechanism and sites of oxidation, degradation of the oxidized enzyme, and inactivation by glycerol, EDTA, and thiol protecting agents.

Acetylglutamate and ATP accelerate the oxidative inactivation of carbamoyl phosphate synthetase I by mixtures of Fe3+, ascorbate, and O2, but the mechanism of the inactivation differs with each ligand. In the presence of acetylglutamate, MgATP prevents, Mg2+, Mn2+, and catalase have no effect, and EDTA increases the inactivation, and the two phosphorylation steps of the enzyme reaction are lost simultaneously. The inactivation appears to be mediated by dehydroascorbate and is associated with the reversible oxidation of the highly reactive cysteines 1327 and 1337 and with oxidation of non-thiolic groups in the second 40-kDa domain (the enzyme consists of 4 domains of 40, 40, 60, and 20 kDa, from the amino terminus). The data are consistent with oxidation of groups at or near the site for ATPA (ATPA yields Pi; ATPB yields carbamoyl phosphate), and with the location of this site at the interphase between the second 40-kDa and the COOH-terminal domains. The oxidative inactivation promoted by ATP is inhibited by Mg2+, Mn2+, catalase, and EDTA, is not mediated by dehydroascorbate, and is not associated with oxidation of cysteines 1327 and 1337. Groups in the 60-kDa domain are oxidized. The phosphorylation step involving ATPB is lost preferentially, and the inactivation and the binding of ATPB exhibit the same dependency on the concentration of ATP. The results indicate that the oxidation is catalyzed by FeATP bound at the site for ATPB and support the binding of ATPB in the 60-kDa domain. We also demonstrate that mercaptoethanol, reducing impurities in glycerol, and dithioerythritol, in the presence of EDTA, replace ascorbate in the oxidative system. In addition, we study the influence of the oxidation on the degradation of the enzyme by rat liver lysosomes, mitochondria, and cytosol.

Adenosine Triphosphate↗

PubMed1993

Peracid oxidation of an N-hydroxyguanidine compound: a chemical model for the oxidation of N omega-hydroxyl-L-arginine by nitric oxide synthase.

Arginine is oxidized by a class of enzymes called the nitric oxide synthases (NOS) to generate citrulline and, presumably, nitric oxide (.NO). N-Hydroxylation of a guanidinium nitrogen of arginine to generate N-hydroxyarginine (NOHA) has been shown to be a step in the biosynthesis of .NO. In an effort to elucidate the mechanism by which further oxidation of NOHA occurs, the oxidation of a model N-hydroxyguanidine compound by several peracids was studied in depth. This oxidative chemistry is a possible model for the enzymatic process since the corresponding urea (or citrulline equivalent product) is obtained along with an oxidized nitrogen species. The oxidized nitrogen product was, however, not .NO but rather HNO. .NO generation in this chemical system and in the enzymatic process would require another one-electron oxidation. The mechanistic details of this are further discussed.

Amidines↗

PubMed2006

Structure and oxidation state of silica-supported manganese oxide catalysts and reactivity for acetone oxidation with ozone.

Silica-supported manganese oxide catalysts with loadings of 3, 10, 15, and 20 wt % (as MnO2) were characterized with use of X-ray absorption spectroscopy and X-ray diffraction (XRD). The edge positions in the X-ray absorption spectra indicated that the oxidation state for the manganese decreased with increasing metal oxide loading from a value close to that of Mn2O3 (+3) to a value close to that of Mn3O4 (+2(2)/3). The XRD was consistent with these results as the diffractograms for the supported catalysts of higher manganese oxide loading matched those of a Mn3O4 reference. The reactivity of the silica-supported manganese oxide catalysts in acetone oxidation with ozone as an oxidant was studied over the temperature range of 300 to 600 K. Both oxygen and ozone produced mainly CO2 as the product of oxidation, but in the case of ozone the reaction temperature and activation energy were significantly reduced. The effect of metal oxide loading was investigated, and the activity for acetone oxidation was greater for a 10 wt % MnOx/SiO2 catalyst sample compared to a 3 wt % MnOx/SiO2 sample.

Journal Article↗

PubMed2005

Nebivolol decreases oxidative stress in essential hypertensive patients and increases nitric oxide by reducing its oxidative inactivation.

OBJECTIVE: To obtain further insight into the mechanism underlying the vasodilator effect of nebivolol. Since oxidative inactivation of nitric oxide (NO) is regarded as an important cause of its decreased biological activity, we studied (1) the effect of nebivolol on some oxidative parameters in essential hypertensive patients; (2) the effect of plasma of nebivolol-treated patients on reactive oxygen species production and NO availability in endothelial cells. METHODS: A total of 20 healthy subjects and 20 matched essential hypertensive patients treated with atenolol or nebivolol according to a double-blind, randomized design participated in the study. We measured low-density lipoprotein (LDL) and plasma hydroperoxides, 8-isoprostanes, oxidized LDL, susceptibility of LDL to oxidation (lag phase) and LDL vitamin E and the effect of plasma of nebivolol- and atenolol-treated patients on reactive oxygen species production and NO availability in endothelial cells exposed to oxidative stress. RESULTS: In hypertensive patients, nebivolol and atenolol significantly reduced blood pressure values after 4 weeks of treatment. Plasma and LDL hydroperoxides, plasma 8-isoprostanes, plasma ox-LDL and LDL lag phase were significantly improved only in the patients receiving nebivolol compared with the atenolol group. Similarly there was a reduction of reactive oxygen species (ROS) and O2*- concentration in endothelial cells exposed to oxidative stress after incubation of the cells with plasma of the patients enrolled in the trial only in the patients receiving nebivolol compared to atenolol group. Furthermore, the reduction of basal and stimulated NO induced by oxidative stress in endothelial cells was significantly lower in the patients receiving nebivolol compared to atenolol group. CONCLUSIONS: The findings of the present study indicate that nebivolol, through its antioxidant properties, increases NO also by decreasing its oxidative inactivation.

Antihypertensive Agents↗

PubMed2002

Characteristics of the surface oxides on turned and electrochemically oxidized pure titanium implants up to dielectric breakdown: the oxide thickness, micropore configurations, surface roughness, crystal structure and chemical composition.

Titanium implants have been used widely and successfully for various types of bone-anchored reconstructions. It is believed that properties of oxide films covering titanium implant surfaces are of crucial importance for a successful osseointegration, in particular at compromized bone sites. The aim of the present study is to investigate the surface properties of anodic oxides formed on commercially pure (c.p.) titanium screw implants as well as to study 'native' oxides on turned c.p. titanium implants. Anodic oxides were prepared by galvanostatic mode in CH3COOH up to the high forming voltage of dielectric breakdown and spark formation. The oxide thicknesses, measured with Auger electron spectroscopy (AES), were in the range of about 200-1000 nm. Barrier and porous structures dominated the surface morphology of the anodic film. Quantitative morphometric analyses of the micropore structures were performed using an image analysis system on scanning electron microscopy (SEM) negatives. The pore sizes were < or = 8 microm in diameter and had 1.27-2.1 microm2 opening area. The porosity was in the range of 12.7-24.4%. The surface roughness was in the range of 0.96-1.03 microm (Sa), measured with TopScan 3D. The crystal structures of the titanium oxide were amorphous, anatase, and a mixtures of anatase and rutile type, as analyzed with thin-film X-ray diffractometry (TF-XRD) and Raman spectroscopy. The chemical compositions consisted mainly of TiO2, characterized with X-ray photoelectron spectroscopy (XPS). The native (thermal) oxide on turned implants was 17.4 nm (+/- 6.2) thick and amorphous. Its chemical composition was TiO2. The surface roughness had an average height deviation of 0.83 microm (Sa). The present results are needed to elucidate the influence of the oxide properties on the biological reaction. The results of animal studies using the presently characterized surface oxides on titanium implants will be published separately.

Crystallography, X-Ray↗

PubMed2005

Unique oxidation reaction of amides with pyridine-N-oxide catalyzed by ruthenium porphyrin: direct oxidative conversion of N-acyl-L-proline to N-acyl-L-glutamate.

Oxidations of alkanes, alkenes, and aromatic rings with pyridine N-oxides are efficiently catalyzed by ruthenium porphyrins under mild conditions. We show here that the oxidation of N-acyl cyclic amines with RuIVtetraarylporphyrin dichloride-2,6-substituted pyridine N-oxides directly gives N-acyl amino acids in modest to good yield via oxidative C-N bond cleavage. N-Acylpyrrolidines and N-acylpiperidines were converted to N-acyl-gamma-aminobutyric acids and N-acyl-delta-aminovaleric acids, respectively. This type of reaction is a novel one in which the C-N bond is cleaved selectively at the less substituted carbon. Notably, the proline residue in proline-containing peptides was selectively converted to glutamate. A large intramolecular kinetic isotope effect (kH/kD = 9.8) was observed in the oxidation of N-benzoyl[2,2,-d2]pyrrolidine, indicating that the reaction should involve an alpha-hydrogen atom abstraction process as the rate-determining step. N-Acylcarbaldehyde, the putative intermediate ring-opened form of alpha-hydroxylated N-acyl cyclic amine, was readily oxidized with the oxidizing system to afford the corresponding N-acylamino acid in good yield. Further, lactams (1-methyl-2-pyrrolidone and 1-methyl- 2-piperidone) were also oxidized to give the corresponding imides (1-methylsuccinimide and 1-methylpiperidine-2,6-dione).

Amines↗

PubMed1993

The contribution of glycolysis, glucose oxidation, lactate oxidation, and fatty acid oxidation to ATP production in isolated biventricular working hearts from 2-week-old rabbits.

Immediately after birth, glycolysis and lactate oxidation are the major source of ATP production in the rabbit heart. Although the ability of heart to oxidize fatty acid increases within days, glucose oxidation rates remain low in the first week after birth. To further examine the changes in energy substrate use in the newborn period, we developed a right and left ventricular isolated working heart model, in which 2-wk-old rabbit hearts were perfused with buffer containing 11 mM glucose, 0.8 mM palmitate, 0.5 mM lactate, and 100 microU/mL insulin. Hearts were perfused at a 7.5 mm Hg left atrial preload, a 4.5 mm Hg superior vena cava preload, a 30 mm Hg aortic afterload, and a 4.5 mm Hg pulmonary artery afterload. Glycolytic rates [measured as 3H2O production from (5-3H)-glucose] were 791 +/- 108 nmol/g dry weight.min-1 (mean +/- SEM). Oxidation rates of glucose, lactate, and palmitate (measured as 14CO2 production from 14C substrates) were 94 +/- 15, 126 +/- 13, and 60 +/- 8 nmol/g dry weight.min-1, respectively. In these hearts, the majority of ATP production derived from exogenous sources was obtained from fatty acid oxidation (52%), whereas 11, 23, and 15% of ATP requirements were derived from glycolysis, glucose oxidation, and lactate oxidation, respectively. These studies demonstrate that by 2 wks of age in rabbits, fatty acids are the major source of energy in the heart. However, although the contribution of glucose oxidation to ATP production has increased compared with 1- or 7-d-old rabbit hearts, glucose oxidation rates are still low compared with adult hearts.

Adenosine Triphosphate↗

PubMed1976

[Studies on high temperature oxidation of noble metal alloys for dental use (I). Formation of oxide layers and oxidation rate (author's transl)].

Eight commercial and two experimental alloys were examined. The cast specimens were polished metallographically and oxidized at 700 degrees and 800 degrees C in air. An electron probe X-ray microanalyser and a microthermobalance were employed to investigate the oxidation behavior of the alloys. The results obtained were as follows: 1. The copper in the alloys was selectively oxidized and the scales formed on the alloys consisted of two layers, CuO overlying Cu2O. 2. The oxide particles in the internal oxidation zone (subscale) on the alloys containing only Cu as the base metal were Cu2O and on the alloys containing Zn, Cd, and Ni with Cu were ZnO, CdO, and NiO, respectively. 3. The size of the ZnO and CdO particles in the subscale increased with the penetration into the specimen. 4. The ZnO particles in the metal-subscale interface showed preferential precipitation at the grain boundaries. 5. When the oxide particles in the subscale did not develop remarkably, the oxidation rate at constant temperature conformed with the parabolic law. 6. In the 18 carat gold alloy, the oxidation rate at 800 degrees C was about 10 times that at 700 degrees C. 7. Owing to preferential oxidation of the Cu in the alloys, Cu concentration in the outer layer of the metal decreased remarkably and Au, Pt, Ag and Pd concentration increased.

Copper↗

PubMed1997

Nitric oxide and acetaminophen-mediated oxidative injury: modulation of interleukin-1-induced nitric oxide synthesis in cultured rat hepatocytes.

The role of endogenous hepatocyte synthesis of nitric oxide (NO) in states of oxidative stress is largely unknown. In a model of rat hepatocytes in primary culture, NO production was induced by exposure to interleukin-1beta (IL-1beta, 50 ng/ml). Acetaminophen-mediated oxidative injury was analyzed in unstimulated and stimulated hepatocytes in the presence and absence of N-methyl-L-arginine, a substrate inhibitor of NO synthesis (100 microM). Inhibition of NO synthesis was associated with exacerbation of acetaminophen-mediated oxidative injury. This effect was independent of guanylyl cyclase and cytochrome P450 activity. In addition, oxidative stress was associated with augmentation of interleukin-1beta-induced NO synthesis. Elevated NO synthesis occurred in parallel with increased inducible NO synthase (iNOS) enzyme activity and mass, steady-state levels of iNOS mRNA, increased transcription of the iNOS gene, and increased iNOS promoter activity. These effects were abrogated in the presence of antioxidants, suggesting that oxidative stress augments NO synthesis through a promoter-specific transcriptional regulatory mechanism. Thus, in conditions where oxidative injury may be a component of the overall proinflammatory state, induction of iNOS with subsequent elaboration of NO and augmentation of NO production may serve as an hepatoprotective mechanism against oxidative injury.

Acetaminophen↗