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1. |
Commentary Salicylate Trapping of -OH as a Tool for Studying Post-Ischemic Oxidative Injury in the Isolated Rat Heart |
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Free Radical Research,
Volume 21,
Issue 6,
1994,
Page 355-370
PowellSaul R.,
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摘要:
The use of salicylate as a chemical trap for -OH represents a simple and convenient alternative to the use of spin trapping techniques to study oxidative injury in isolated perfused organs. In these systems, salicylate is included in the perfusion buffer at concentrations ranging from 0.1 to 2mM depending on the detection apparatus employed. In our studies, we have used a coulometric detector, which has a theoretical efficiency of 100% as compared to 1–5% for the standard glassy carbon electrode. We have been able to generate reproducible results by inclusion of only 100μM salicylate, a concentration demonstrated not to affect pre- or post-ischemic cardiac function. In initial studies, we observed an increase in perfusate 2,5-dihydroxybenzoic acid consistent with an early post-ischemic burst of -OH, not unlike that reported using spin trapping techniques. Since then we and others have used this technique to examine possible relationships between -OH formation and treatments that alter post-ischemic cardiac functional recovery. For example, preischemic loading of hearts with copper results in increases in postischemic dysfunction and LDH release that were associated with an increase in 2,5-dihydroxybenzoate and by inference, -OH formation. Alternatively, we have reported that the nitroxide spin label, TEMPO, reputed to be a superoxide dismutase mimetic, decreased post-ischemic arrhythmias and 2,5-dihydroxybenzoate formation. Most recently, we have observed that preischemic loading of hearts with zinc-bis-histidinate results in improved post-ischemic cardiac function and decreased LDH release; changes that were associated with decreased 2,5-dihydroxybenzoate formation. These studies indicate that under certain conditions, salicylate is a valuable alternative to spin trapping techniques to probe the role of -OH in cardiac oxidative injury, particularly when applied to the isolated perfused heart preparation.
ISSN:1071-5762
DOI:10.3109/10715769409056588
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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2. |
Inhibitory Effect of Bifemelane on Superoxide Generation by Activated Neutrophils Measured Using a Simple Chemiluminescence Method |
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Free Radical Research,
Volume 21,
Issue 6,
1994,
Page 371-376
YoshidaToshihiko,
SotomatsuAkemi,
TanakaMakoto,
HiraiShunsaku,
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摘要:
We evaluated the effect of 4-(2-benzylphenoxy)-N-methylbutylamine hydrochloride (bifemelane hydrochloride) on superoxide production by human neutrophils using an MCLA-dependent chemiluminescence assay. Bifemelane hydrochloride dose-dependently inhibited superoxide production by neutrophils stimulated with phorbol myristate acetate, opsonized zymosan, or N-formyl-methionyl-leucyl-pheny-lalanine, while it had no effect on superoxide production by a hypoxanthine-xanthine oxidase system. These results indicate that bifemelane hydrochloride does not have a scavenging effect, but has an inhibitory effect on superoxide generation by neutrophils. Although this drug is commonly used for treating chronic cerebral infarction, it may also have a protective effect on acute ischemia/reperfusion injury.
ISSN:1071-5762
DOI:10.3109/10715769409056589
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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3. |
Sequential Oxidative Damage, and Changes in Iron-Binding and Iron-Oxidising Plasma Antioxidants During Cardiopulmonary Bypass Surgery |
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Free Radical Research,
Volume 21,
Issue 6,
1994,
Page 377-385
PepperJohn R.,
MumbySharon,
GutteridgeJohn M.C.,
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摘要:
Cardiopulmonary bypass patients undergoing heart valve replacement surgery appear to be under oxidative stress, when compared with normal healthy controls, by showing increased levels of protein and lipid damage. During bypass surgery two further episodes of oxidative stress occur. The first is seen when patients are placed on extracorporeal blood circulation and oxygenation which results in a rise in lipid peroxides and thiobarbituric acid-reactive substances. The second phase of oxidative stress occurs during reperfusion of the myocardium following removal of the aortic cross clamp. Coincident with evidence of increased oxidative damage to lipids during these latter phases of oxidative stress were decreases in plasma iron-binding and iron-oxidising antioxidant activities.
ISSN:1071-5762
DOI:10.3109/10715769409056590
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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4. |
Free Radical Inactivation of Rabbit Muscle Creatine Kinase: Catalysis by Physiological and Hydrolyzed ICRF-187 (ICRF-198) Iron Chelates |
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Free Radical Research,
Volume 21,
Issue 6,
1994,
Page 387-397
ThomasCarin,
CarrAnitra C.,
WinterbournChristine C.,
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摘要:
Creatine kinase is a sulfhydryl containing enzyme that is particularly susceptible to oxidative inactivation. This enzyme is potentially vulnerable to inactivation under conditions when it would be used as a diagnostic marker of tissue damage such as during cardiac ischemia/reperfusion or other oxidative tissue injury. Oxidative stress in tissues can induce the release of iron from its storage proteins, making it an available catalyst for free radical reactions. Although creatine kinase inactivation in a heart reperfusion model has been documented, the mechanism has not been fully described, particularly with regard to the role of iron. We have investigated the inactivation of rabbit muscle creatine kinase by hydrogen peroxide and by xanthine oxidase generated superoxide or Adriamycin radicals in the presence of iron catalysts. As shown previously, creatine kinase was inactivated by hydrogen peroxide. Ferrous iron enhanced the inactivation. In addition, micromolar levels of iron and iron chelates that were reduced and recycled by superoxide or Adriamycin radicals were effective catalysts of creatine kinase inactivation. Of the physiological iron chelates studied, Fe(ATP) was an especially effective catalyst of inactivation by what appeared to be a site-localized reaction. Fe(ICRF-198), a non-physiological chelate of interest because of its putative role in alleviating Adriamycin-induced cardiotoxicity, also catalyzed the inactivation. Scavenger studies implicated hydroxyl radical as the oxidant involved in iron-dependent creatine kinase inactivation. Loss of protein thiols accompanied loss of creatine kinase activity. Reduced glutathione (GSH) provided marked protection from oxidative inactivation, suggesting that enzyme inactivation under physiological conditions would occur only after GSH depletion.
ISSN:1071-5762
DOI:10.3109/10715769409056591
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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5. |
Enhancement of Nitrogen Dioxide-Induced Lipid Peroxidation and Dna Strand Breaking by Cysteine and Glutathione |
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Free Radical Research,
Volume 21,
Issue 6,
1994,
Page 399-408
KikugawaKiyomi,
HiramotoKazuyuki,
OkamotoYutaka,
KoYo,
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摘要:
Nitrogen dioxide less than 100 ppm in air induced lipid peroxidation of liposome composed of l-palmitoyl-2-arachidonylphosphatidylcholine as assessed by thiobarbituric acid reactivity. The nitrogen dioxide-induced lipid peroxidation was enhanced by cysteine, glutathione and bovine serum albumin. While the activity of nitrogen dioxide in air to induce single strand breaks of supercoiled plasmid DNA was low, the breaking was remarkably enhanced by cysteine, glutathione and bovine serum albumin. ESR spin trapping using 5,5-dimethyl-1-pyrroline N-oxide showed that certain strong oxidant(s) were generated by interaction of nitrogen dioxide and cysteine. The spin trapping using 3,5-dibromo-4-nitrosobenzene-sulfonate suggested that sulfur-containing radicals were generated by interaction of nitrogen dioxide and cysteine or glutathione. Hence, certain sulfur-containing radicals generated by the interaction which could effectively induce lipid peroxidation and DNA strand breaks.
ISSN:1071-5762
DOI:10.3109/10715769409056592
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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6. |
Antioxidant Properties of Plastoquinol and Other Biological Prenylquinols in Liposomes and Solution |
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Free Radical Research,
Volume 21,
Issue 6,
1994,
Page 409-416
KrukJerzy,
SchmidGeorg H.,
StrzalkaKazimierz,
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摘要:
Oxidation of biological prenylquinols, like plastoquinol-9 (PQH2-9), ubiquinol-10 (UQH2-10), reduced vitamins K1(VK1H2) and K2(VK2H2),α-tocopherol quinol (α-TQH2) andα-tocopherol (α-T) was followed by their fluorescence during sonication of egg yolk lecithin/prenylquinol liposomes. The order of magnitude of oxidation of the prenylquinols by free radicals generated during sonication wasVK2H2VK1H2α-TQH2α-T. It was shown that egg yolk lecithin undergoes degradation even when sonicated briefly under atmosphere of nitrogen and at 0°C. A kinetic study of free radical scavenging action of the prenylquinols in solvents of different polarity was performed. The pseudo-first-order rate constants, k, for the reaction of the prenylquinols with 1,1-diphenyl-2-picryl-hydrazyl (DPPH) in hexane showed that their scavenging activity changes in the order
ISSN:1071-5762
DOI:10.3109/10715769409056593
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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7. |
Antioxidant Activity of Saliva and Periodontal Disease |
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Free Radical Research,
Volume 21,
Issue 6,
1994,
Page 417-425
MooreSuzanne,
CalderKaren A.C.,
MillerNicholas J.,
RiceCatherine A.,
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摘要:
The antioxidant activity of saliva has been investigated in 28 apparently healthy individuals and seven dental patients with periodontal disease. The results show that the major aqueous antioxidant component of whole saliva is uric acid, with lesser contributions from ascorbic acid and albumin. All are present at lower concentrations than those found in the plasma water. The total antioxidant activity (TAA) of saliva correlates (r2= 0.972) with the concentration of uric acid, which contributes more than 70% of the TAA. Stimulation of salivary flow is associated with increased production of antioxidants. The antioxidant potential of saliva does not appear to be compromised in patients with periodontal disease but this may relate to the antioxidant flow from the gingival crevicular fluid.
ISSN:1071-5762
DOI:10.3109/10715769409056594
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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8. |
Prevention of Carbon Tetrachloride-Induced Lipid Peroxidation in Liver Microsomes from Dehydroepiandrosterone-Pretreated Rats |
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Free Radical Research,
Volume 21,
Issue 6,
1994,
Page 427-435
AragnoManuela,
TamagnoElena,
PoliGiuseppe,
BoccuzziGiuseppe,
BrignardelloEnrico,
DanniOliviero,
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摘要:
Dehydroepiandrosterone (DHEA), a lipid soluble steroid, administered to rats (100 mg/kg b.wt) by a single intraperitoneal injection, increases to twice its normal level in the liver microsomes. Microsomes so enriched become resistant to lipid peroxidation induced by incubation with carbon tetrachloride in the presence of a NADPH-regenerating system: also the lipid peroxidation-dependent inactivation of glucose-6-phosphatase and gamma-glutamyl transpetidase due to the haloalkane are prevented. Noteworthy, the liver microsomal drug-metabolizing enzymes and in particular the catalytic activity of cytochrome P450IIE1, responsible for the CCl4-activation, are not impaired by the supplementation with the steroid. Consistently, in DHEA-pretreated microsomes the protein covalent binding of the trichloromethyl radical (CCl3°), is similar to that of not supplemented microsomes treated with CCl4. It thus seems likely that DHEA protects liver microsomes from oxidative damage induced by carbon tetrachloride through its own antioxidant properties rather than inhibiting the metabolism of the toxin.
ISSN:1071-5762
DOI:10.3109/10715769409056595
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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9. |
Forthcoming Meeting 1994 |
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Free Radical Research,
Volume 21,
Issue 6,
1994,
Page 437-438
AragnoManuela,
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ISSN:1071-5762
DOI:10.3109/10715769409056596
出版商:Taylor&Francis
年代:1994
数据来源: Taylor
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