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At least 19 recordsLinked to original sources
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↗
PubMed1976

Carcinogenicity of Benzo(a)pyrene and dusts in the hamster lung (instilled intratracheally with titanium oxide, aluminum oxide, carbon and ferric oxide).

The possible carcinogenic or fibrogenic effects of intratracheal instillation of a polycyclic hydrocarbon, benzo(a) pyrene (B(a)P), alone or in combination with several dusts - titanium dioxide (TiO2), aluminum oxide (Al2O3), carbon (C), and ferric oxide (Fe3O3) - were investigated in hamsters. When administered alone, the dusts induced interstitial cell proliferation, bronchial epithelial alterations and a few granulomatous changes in the pulmonary system, but no tumors. B(a)P alone induced only two tracheal papillomas. However, combined treatment with B(a)P and the dusts caused a number of tumors, dependent upon the dust used. B(a)P plus TiO2 in a small particle size (below 0.5mu) induced papillomas, squamous cell carcinomas and a few adenomas and adenocarcinomas of the larynx, trachea and lungs. These were morpholoigcally similar to neoplasms found after B(a)P and Fe2O3 treatment. B(a)P, combined with C or Al2O3, induced mainly laryngeal and tracheal papillomas. B(a)P- and C-treated hamsters also showed a few lung adenocarcinomas.

Adenocarcinoma↗
PubMed1978

Contribution of omega-oxidation to fatty acid oxidation by liver of rat and monkey.

Contributions of omega-oxidation to overall fatty acid oxidation in slices from livers of ketotic alloxan diabetic rats and of fasted monkeys are estimated. Estimates are made from a comparison of the distribution of 14C in glucose formed by the slices from omega-14C-labeled compared to 2-14C-labeled fatty acids of even numbers of carbon atoms and from [1-14C]acetate compared to [2-14C]acetate. These estimates are based on the fact that 1) the dicarboxylic acid formed via omega-oxidation of a omega-14C-labeled fatty acid will yield [1-14C]acetate and [1-14C]succinate on subsequent beta-oxidation, if beta-oxidation is assumed to proceed to completion; 2) only [2-14C]acetate will be formed if the fatty acid is metabolized solely via beta-oxidation; and 3) 14C from [1-14C]acetate and [1-14C]succinate is incorporated into carbons 3 and 4 of glucose and 14C from [2-14C]acetate is incorporated into all six carbons of glucose. From the distributions found, the contribution of omega-oxidation to the initial oxidation of palmitate by liver slices is estimated to between 8% and 11%, and the oxidation of laurate between 17% and 21%. Distributions of 14C in glucose formed from 14C-labeled palmitate infused into fasted and diabetic rats do not permit quantitative estimation of the contribution of omega-oxidation to fatty acid oxidation in vivo. However, the distributions found also indicate that, of the fatty acid metabolized by the whole animal in the environment of glucose formation, at most, only a minor portion is initially oxidized via omega-oxidation. As such, omega-oxidation cannot contribute more than a small extent to the formation of glucose.

Acetates↗
PubMed1978

Oxidized cholesterol bilayers. Dependence of electrical properties on degree of oxidation and aging.

Black lipid membranes made from oxidized cholesterol were examined for their specific resistance, capacitance, and physical stability, as a function of cholesterol oxidation time and of age. Membranes formed from cholesterol oxidized in n-octane were not physically stable even after 7 h of oxidation unless they were aged for at least a month. Membranes formed from cholesterol oxidized in decane and tetradecane (1 : 1) were stable immediately after 2--6 h of oxidation. Oxidation times outside this range produced unstable membranes. After 1 month storage, membranes from cholesterol solutions oxidized in decane and tetradecane from 0.75--3 h were stable. After 11 months, only the 0.75 oxidation time produced stable membranes. Storage in nitrogen retarded the aging process. After initial forming of the membrane, total membrane area and capacity increased and then stabilized, although specific capacity and resistance did not change, indicating inherent stability in the bilayer's intrinsic electrical properties. Bilayers formed soon after cholesterol oxidation had membrane capacity which ranged from 0.42 to 0.55 muF/cm2. Specific membrane resistance ranged initially from 2 . 10(6) to 37 . 10(6) omega/cm2 in 0.2 M NaCl with lower resistances in the more oxidized membranes. With aging, membrane capacity decreased gradually over 11 months to values approaching 0.1 muF/cm2 indicating membrane thickening. Membrane resistance ordinarily decreases with storage time. The rate of these changes with age is dependent on the extent of initial cholesterol oxidation and subsequent oxidation, with long term stability best in the least oxidized membranes.

Cholesterol↗
PubMed1978

The oxidative activities of membrane vesicles from Bacillus caldolyticus. Energy-dependence of succinate oxidation.

1. The properties of membrane vesicles from the extreme thermophile Bacillus caldolyticus were investigated. 2. Vesicles prepared by exposure of spheroplasts to ultrasound contained cytochromes a, b and c, and at 50 degrees C they rapidly oxidized NADH and ascorbate in the presence of tetramethyl-p-phenylenediamine. Succinate and l-malate were oxidized more slowly, and dl-lactate, l-alanine and glycerol 1-phosphate were not oxidized. 3. In the absence of proton-conducting uncouplers the oxidation of NADH was accompanied by a net translocation of H(+) into the vesicles. Hydrolysis of ATP by a dicyclohexylcarbodi-imide-sensitive adenosine triphosphatase was accompanied by a similarly directed net translocation of H(+). 4. Uncouplers (carbonyl cyanide p-trifluoromethoxyphenylhydrazone or valinomycin plus NH(4) (+)) prevented net H(+) translocation but stimulated ATP hydrolysis, NADH oxidation and ascorbate oxidation. The last result suggested an energy-conserving site in the respiratory chain between cytochrome c and oxygen. 5. Under anaerobic conditions the reduction of cytochrome b by ascorbate (with tetramethyl-p-phenylenediamine) was stimulated by ATP hydrolysis, indicating an energy-conserving site between cytochrome b and cytochrome c. However, no reduction of NAD(+) supported by oxidation of succinate, malate or ascorbate occurred, neither did it with these substrates in the presence of ATP under anaerobic conditions, suggesting that there was no energy-conserving site between NADH and cytochrome b. 6. Succinate oxidation, in contrast with that of NADH and ascorbate, was strongly inhibited by uncouplers and stimulated by ATP hydrolysis. These effects were not observed when phenazine methosulphate, which transfers electrons from succinate dehydrogenase directly to oxygen, was present. It was concluded that in these vesicles the oxidation of succinate was energy-dependent and that the reoxidation of reduced succinate dehydrogenase was dependent on the outward movement of H(+) by the protonmotive force. 7. In support of the foregoing conclusion it was shown that the reduction of fumarate by NADH was an energy-conserving process. 8. If the activities of vesicles accurately represent those of the intact organism it appears that in B. caldolyticus the reduction of fumarate to succinate at the expense of reducing equivalents from NADH is energetically favoured over succinate oxidation even under aerobic conditions. This may be related to the need for an ample supply of succinate for haem synthesis in order to provide cytochromes for the organism.

Adenosine Triphosphate↗
PubMed1977

Nitrite and nitric oxide treatment of Helix pomatia hemocyanin: single and double oxidation of the active site.

The reaction of nitrite and nitric oxide with Helix pomatia hemocyanin has been studied. One or both of the two copper ions in the active site can be oxidized, depending upon reaction conditions. The single oxidation of the oxygen binding site can be reversed by reduction with hydroxylamine, and the oxygen binding properties of the protein are simultaneously restored. The experiments, including electron paramagnetic resonance, indicate that nitric oxide is not a ligand of copper in the singly oxidized active site and that the oxidized copper ions is coupled to at least two nitrogen atoms of amino acid residues. The doubly oxidized protein can be reduced to a singly oxidized one with ascorbic acid or hydroxylamine; the latter reagent is again able to reduce the singly oxidized state and to restore the oxygen binding properties.

Animals↗
PubMed1976

[Studies on high temperature oxidation of noble metal alloys for dental use. (II) Effects of high temperature oxidation on casting (author's transl)].

The specimens which were cast from commercial alloys were polished metallographically and then oxidized at 800 degrees C for 1 hour in air. The results obtained were as follows: 1. The reduction rate of Cu aginast the original Cu amount in the alloy is given by the following equation: (see article) where S is surface area of the casting, KW is oxidation rate constant, t is time, Wc is weight of the casting, Ccu is weight percent of Cu, and n is between 1 and 2. 2. Owing to decrease of the Cu concentration in the outer layer of the alloy, the age-hardening did not appear in that layer. 3. Reflexibility of the polished surface of alloys became lower than that of the matrix due to precipitation of the oxide particles. 4. Hardness numbers of the internal oxidation zone (oxide particles, ZnO) decreased to 1/2 of the matrix. 5. The surface roughness of specimens after pickling was affected by the shape of oxide particles in the internal oxidation zone and varied with the different commercial alloys. 6. The dimensional change of casting due to oxidation is given by the following equation: (see article) where sigmacu is density of copper, KW is oxidation rate constant, t is time and n is between 1 and 2.

Copper↗
PubMed1976

[Studies on high temperature oxidation of noble metal alloys for dental use. (III) On high temperature oxidation resistance of noble metal alloys by adding small amounts of alloying elements. (author's transl)].

The previous report pointed out the undesirable effects of high temperature oxidation on the casting. The influence of small separate additions of Zn, Mg, Si, Be and Al on the high temperature oxidation of the noble metal alloys was examined. These alloying elements were chosen because their oxide have a high electrical resistivity and they have much higher affinity for oxygen than Cu. The casting were oxidized at 700 degrees C for 1 hour in air. The results obtained were as follows: 1. The Cu oxides are not observed on the as-cast surface of noble metal alloys containing small amounts of Zn, Mg, Si, Be, and Al. The castings have gold- or silver-colored surface. 2. After heating of the unpolished and polished castings, the additions of Si, Be and Al are effective in preventing oxidation of Cu in the 18 carats gold alloys. Especially the golden surface is obtained by adding Be and Al. But there is no oxidation-resistance on the polished castings in the alloys containing Zn and Mg. 3. The zinc oxide film formed on the as-cast specimen is effective in preventing of oxidation Cu in 18 carats gold alloys. 4. It seems that the addition of Al is most available in dental application.

Aluminum↗
PubMed1978

Interfacial oxidation of alpha-tocopherol and the surface properties of its oxidation products.

dl-alpha-Tocopherol spread on an acidic subphase as a gaseous monolayer was oxidized slowly to a derivative that was identified by thin-layer chromatography as alpha-tocopherylquinone. The derivative generated the same II-A isotherm as alpha-tocopherylquinone. When the subphase contained gold chloride, alpha-tocopherol was oxidized rapidly and quantitatively to alpha-tocopherylquinone. dl-alpha-Tocopherol spread on a basic subphase as a gaseous monolayer was oxidized slowly to a mixture that contained alpha-tocopherol, a quinone, and a nonpolar derivative. The mixture generated a II-A isotherm with an inflection point below the equilibrium spreading pressure of either alpha-tocopherol or alpha-tocopherylquinone. When potassium ferricyanide was added to the alkaline subphase, alpha-tocopherol was oxidized rapidly to a mixture that contained both the nonpolar derivative (major product) and the quinone (minor product). The nonpolar derivative was isolated by thin-layer chromatography and identified as the spirodienone ether by ultraviolet, infrared, and chemical ionization mass spectra. The spirodienone ether had a low equilibrium spreading pressure that explained the inflection point in the II-A isotherm generated by alpha-tocopherol on an alkaline subphase. Surface area data showed that dl-alpha-tocopherol formed immiscible films with stearyl alcohol and miscible films with oleyl alcohol. II-A isotherms showed that alpha-tocopherol in both immiscible and miscible mixtures was oxidized rapidly on an alkaline potassium ferricyanide subphase to the spirodienone ether. Collapse pressure data showed that the spirodienone ether formed an immiscible film with stearyl alcohol and a miscible film with oleyl alcohol. Interfacial oxidation experiments showed that alpha-tocopherol is oxidized either to tocopherylquinone (acidic subphase) or to the spirodienone ether (alkaline subphase). The natural occurrence of both tocopherylquinone and the spirodienone ether suggests that several types of oxidant stress are found in biological systems. One type of oxidant stress may involve the peroxy radical generating tocopherylquinone; a second type may involve hydroxyl radical-hydroxide ion generating the spirodienone ether.

Fatty Alcohols↗
PubMed1978

Comparative biochemistry of beta-oxidation. An investigation into the abilities of isolated heart mitochondria of various animal species to oxidize long-chain fatty acids, including the C22:1 monoenes.

Rates of acylcarnitine oxidation by isolated heart mitochondria from various animal species were measured polarographically, and by using a spectrophotometric assay [see Osmundsen & Bremer (1977) Biochem. J. 164, 621-633]. Polarographic measurements do not give a correct guide to abilities to beta-oxidize very-long-chain acylcarnitines, in particular C22:1 fatty acylcarnitines. 2. No significant species differences were detected in the abilities to beta-oxidize various C22:1 fatty acylcarnitines. Significant species differences were, however, detected when rates of beta-oxidation were correlated with rates of respiration brought about by very-long-chain acylcarnitines. We concluded that some aspects of oxidative metabolism (possibly the oxidation of tricarboxylic acid-cycle intermediates) are inhibited by very-long-chain fatty acids in some species (e.g. the rat and the cat but not in others (e.g. the pig and the rabbit). 3. It is proposed that the pattern of variation of rates of oxidation of various acylcarnitines (as measured spectrophotometrically) of various chain lengths can be used as a guide to the chain-length specificities of the acyl-CoA dehydrogenases of beta-oxidation (EC 1.3.99.3).

Animals↗
PubMed1975

Oxidizing action of purine N-oxide esters.

A technique involving O-acetylation of purine N-oxide derivatives in buffered aqueous solutions has permitted studies of the reactivity of many compounds for which the O-acetyl derivatives are not otherwise available. The oxidizing properties of a variety of N-acetoxypurines have been measured through their ability to oxidize iodide ion ot iodine, a reaction which is representative of a more general oxidizing ability. Those esters that oxidize iodide ion also catalyze the autoxidation of sulfite, a property characteristic of radicals. The same esters also oxidize cysteine to cysteic acid and tryptophan, tyrosine, and uric acid to yet uncharacterized products. Their oxidizing reactivity was compared with the ability of the same esters to react as electrophiles in another assay that measured the rate of formation of pyridine substitution products. The sulfate ester of 3-hydroxyxanthine has been synthesized. Its reactivity is qualitatively the same as that of 3-acetoxyxanthine but proceeds at a higher rate. Syntheses of S-(8-xanthyl)-N-acetylcysteine, 8-(2-hydroxyethylthio)xanthine, and 1-methyl-8-mehtylmercaptoguanine are also described.

Acetylation↗
PubMed1979

Flavoprotein-linked substrate oxidation in preparations of hamster brown adipocytes. A discrimination between internally and externally oxidized substrates.

Noradrenaline-stimulated oxidative metabolism in isolated hamster brown fat cells is very reproducible between different cell preparations, 565 +/- 81 (S.D.) nmol O/min per 10(6) cells (n = 25). In contrast, the oxygen consumption rate induced by the addition of succinate or sn-glycerol 3-phosphate strongly varies between different cell preparation, although these substances have been reported to be potent substrates for isolated hamster brown fat cells. By filtration and by successive washings we demonstrate that the flavoprotein-linked substrate oxidation is mainly dependent on extracellular succinate and sn-glycerol 3-phosphate-oxidizing enzymes. These enzymes originate from damaged and broken cells and are present in different amounts in different cell preparations. In discriminating between intra- and extracellular succinate oxidation 5,5'- dithiobis(2-nitrobenzoate) is used as an inhibitor of the extracellular portion. This application of 5,5'-dithiobis(2-nitrobenzoate) ought to be useful also in other cell or tissue preparations. Added succinate can, however, be oxidized by the intact brown adipocyte but at very low rate, probably as a result of a limited transport rate over the membrane(s). In the presence of noradrenaline, added succinate can potentiate the noradrenaline-inducible oxygen consumption by catalytically increasing the oxidative capacity of the citric acid cycle. Our conclusions is that the only effectors which significantly increase oxidative metabolism in intact isolated hamster brown fat cells are catecholamines and free fatty acids. Provided the cells are uncoupled, also pyruvate can function as substrate for these cells.

Adipose Tissue, Brown↗
PubMed1977

Monoethlenic C20 and C22 fatty acids in marine oil and rapeseed oil. Studies on their oxidation and on their relative ability to inhibit palmitate oxidation in heart and liver mitochondria.

1. Carnitine esters of erucic acid (22:1 n-9 cis), cetoleic acid (22:1 n-11 cis), brassidic acid (22:1 n-9 trans), gadoleic acid (20:1 n-9 cis) and oleic acid (18:1 n-9 cis) have been compared as mitochondrial substrates and as inhibitors of palmitoylcarnitine oxidation in heart and liver mitochondria. 2. Both the rate of intramitochondrial-CoA acylation and the rate of beta-oxidation decreases as the chain length increases from C18 to C22. There are no significant differences among the three C22 isomers as oxidizable substrates. 3. All the tested acylcarnitines inhibit palmitoylcarnitine oxidation. The C18 and C20 acylcarnitines inhibit by virtue of being competing substrates; i.e. the respiration is not inhibited. The C22-isomers inhibit also respiration; this shows that the inhibition of palmitolycarnitine oxidation is not compensated for by oxidation of C22-acylcarnitines. Brassidoylcarnitine inhibits the oxidation of palmitoylcarnitine and respiration less than erucoyl-and cetoleoylcarnitine. The different behaviour of the C22-isomers is probably due to the difference in their competitive properties with respect to long-chain acyl-CoA dehydrogenase. 4. All C22 acylcarnitines seem to be relatively better oxidized in the liver than in the heart mitochondria while their inhibitory effect on the usage of the radioactive palmitoylcarnitine is very similar. 5. Palmitoylcarnitine inhibits almost completely the "endogenous" formation of acetyl-CoA presumably from malate via pyruvate in the liver mitochondria while the C22-acylcarnitines cause only a partial inhibiton of this acetyl-CaO formation.

Animals↗
PubMed1977

A spectrophotometric procedure for rapid and sensitive measurements of beta-oxidation. Demonstration of factors that can be rate-limiting for beta-oxidation.

1. A spectrophotometric direct-reading assay for measurements of beta-oxidation by intact mitochondria is described. The procedure relies on the ability of ferricyanide to trap reducing equivalents generated by the acyl-CoA dehydrogenases (EC 1.3.99.3). The reduction of ferricyanide was recorded by using a dual-wavelength spectrophotometer. 2. Oxaloacetate or acetoacetate was used to stimulate the rate of beta-oxidation by rotenone-blocked mitochondria. Although both were effective with rat liver mitochondria, oxaloacetate gave about 75% more stimulation. With heart or kidney mitochondria, only oxaloacetate gave marked stimulation. Acetoacetate had no stimulatory effect with heart mitochondria, but a small stimulatory effect on the rate of beta-oxidation by kidney mitochondria. 3. The stoicheiometry of beta-oxidation-dependent reduction of ferricyanide was examined, and good correlations were found between experimental and theoretical amounts of ferricyanide reduced. 4. Ferricyanide appears as efficient a final electron acceptor as O2. With ferricyanide the rate of beta-oxidation by heart mitochondria can be measured without interference from the oxidation of tricarboxylic acid-cycle intermediates.

Acetoacetates↗