摘要:

Glutathione serves as an important intracellular defence against reactive oxygen metabolites and has been shown to be depleted from a number of tissues upon oxidative stress. In the present study we have investigated the levels of total glutathione (reduced + oxidized) in skeletal muscle of the rat after prolonged ischema and reperfusion with and without treatment with hyperbaric oxygen (HBO) for the initial 45 minutes immediately following reperfusion. A tourniquet model for temporary, total ischemia was used, in which one hind leg was made ischemic for 3 or 4 hours. Muscle biopsies were taken after 5 hours of reperfusion. In postischemic muscle there was a significant decrease of total glutathione compared to control muscle, but in the 3-hour-ischema-groups the loss of total glutathione was less in HBO treated animals than in untreated. HBO treatment also preserved ATP and PCr and decreased edema formation in the postischemic muscle following 3 hours of ischemia and reperfusion when compared to untreated animals. However, after 4 hours of ischemia, HBO treatment failed to improve any of these parameters in the postischemic muscle. Thus, our results demonstrate that HBO treatment lessens the metabolic, ischemic derangements and improves recovery in postischemic muscle after 3 hours of ischemia followed by reperfusion.

ISSN:1071-5762    

DOI:10.3109/10715769509064024

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

The production of singlet oxygen by H2O2disproportionation and via the oxidation of H2O2by NaOCl in a neutral medium was monitored by spin trapping with 2,2,6,6 tetramethyl-4-piperidone (TMPone). The singlet oxygen formed in both reactions oxidized 2,2,6,6 tetramethyl-4-piperidone to give nitroxide radicals. However the production of nitroxide radicals was relatively small considering the concentrations of H2O2and NaOCl used in the reaction systems. Addition of electron donating agents: ascorbate, Fe2+and desferrioxamine leads to an increase in the production of nitroxide radicals. We assumed that a very slow step of the reaction sequence, the homolytic breaking of the O-O bond of N-hydroperoxide (formed as an intermediate product during the reaction of1O2with TMPone) could be responsible for the relatively small production of nitroxide radicals. Electron donating agents added to the reaction system probably raise the rate of the hydroperoxide decomposition by allowing a more rapid heterolytic cleavage of the O-O bond leading to a greater production of nitroxide radicals. The largest effect was observed in the presence of desferrioxamine. Its participation in this process is proved by the concomitant appearance of desferrioxamine nitroxide radicals. The results obtained demonstrate that the method proposed by several authors and tested in this study to detect singlet oxygen is not convenient for precise quantitative studies. The reactivity of TMPone towards O2−7HO2' and 'OH has been also investigated. It has been found that both O2−7HO2' and 'OH radicals formed in a phosphate buffer solution (pH 7.4, 37°C), respectively by a xanthine-oxidase/hypoxanthine system and via H2O2UV irradiation, do not oxidize 2,2,6,6 tetramethyl-4-piperidone to nitroxide radicals.

ISSN:1071-5762    

DOI:10.3109/10715769509064025

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

Pentane and isoprene concentrations were analyzed in single end-expiratory breath samples using gas chromatography. Breath analysis was performed in 15 patients with acute myocardial infarction, 15 patients with stable angina, and 15 healthy control subjects. The two patient groups were well matched for age, sex, smoking habits, hypertension and serum cholesterol levels. There was no significant difference in breath pentane concentration in the acute myocardial infarction group (0.29 + 0.03 nmol/l) (mean + SEM) compared to the group with stable angina (0.31±0.03 nmol/l) or the control group (0.36±0.04 nmol/l). However, breath isoprene concentration was higher (p<0.01) in the acute myocardial infarction group (11.4±1.2 nmol/l), compared to both the stable angina group (7.7±0.5 nmol/l) and the control group (7.1±1.0 nmol/l). There was no difference in either the pentane or isoprene concentrations between the control group and the group with stable angina. Since pentane is thought to be an index of lipid peroxidation, the results do not support the presence of enhanced lipid peroxidation in acute myocardial infarction in the absence of thrombolytic therapy or primary angioplasty. The mechanism responsible for isoprene elevation in acute myocardial infarction is unknown.

ISSN:1071-5762    

DOI:10.3109/10715769509064026

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

Neopterin and its reduced form, 7,8 dihydroneopterin afe pteridines released from macrophages and monocytes when stimulated with interferon gammain vivo.The function of this response is unknown though there is an enormous amount of information available on the use of these compounds as clinical markers of monocyte/macrophage activation. We have found that in vitro 7,8-dihydroneopterin dramatically increases, in a dose dependent manner, the lag time of low density lipoprotein oxidation mediated by Cu++ions or the peroxyl radical generator 2,2′-azobis (2-amidino propane) dihydrochloride (AAPH). 7,8-Dihydroneopterin also inhibits AAPH mediated oxidation of linoleate. The kinetic of the inhibition suggests that 7,8-dihydroneopterin is a potent chain breaking antioxidant which functions by scavenging lipid peroxyl radicals. No anti-oxidant activity was observed in any of the oxidation systems studied with the related compounds neopterin and pterin.

ISSN:1071-5762    

DOI:10.3109/10715769509064027

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

Copper-induced LDL oxidation is characterized by an 'induction phase' (lag phase) during which the endogenous antioxidants are consumed, followed by a 'propagation phase' in which the LDL-associated polyunsaturated fatty acids are oxidized. Oxidation products may play an important role in the propagation of the oxidative process in the arterial intima as they increase the permeability of the damaged endothelium to various plasma components, including LDL. We therefore found it of interest to investigate the kinetics of LDL oxidationin vitrounder conditions where LDL is sequentially exposed to Cu2+-induced oxidation.The results of our studies demonstrate that when native LDL is exposed to copper oxidation in a medium containing oxidized LDL, oxidation of the added LDL may be almost instantaneous. Furthermore, even when native LDL is added to 'oxidizing LDL' towards the end of the lag phase or during the propagation phase it becomes oxidized after a very short lag. This oxidation process, occurring in spite of the possible protective effect of the antioxidants present in the newly added LDL, indicates that although antioxidants prolong the latency period by preventing the formation of active free radicals, when such radicals are present in the system, oxidation propagates. These results lend strong support to the generally accepted paradigm regarding the mechanism of propagation of lipid oxidation.In view of the effect of oxidation products on the permeability of the endothelium, the observed shortening of the lag period may result in a vicious cycle, independent of the LDL-associated antioxidants, leading to continuing oxidation and foam cell formation.

ISSN:1071-5762    

DOI:10.3109/10715769509064028

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

Kinetic modelling overcomes some of the drawbacks of purely intuitive thinking in integrating information accumulated on chemical reactions involved in oxidative stress. However, it is important to assess if current knowledge about the reactions that mediate lipid peroxidation already allows satisfactory modelling of this process in near-to-physiological conditions. In this paper, a set of increasingly complexin vitroexperiments on antioxidants (a-tocopherol and ascorbate) and lipid peroxidation in heterogeneous systems is simulated. Quantitative to semiquantitative agreement is found between experimental and simulation results. In addition, this theoretical analysis provided useful insights, suggested new hypotheses and experiments and pointed out relevant aspects needing further research. The results encourage and serve as partial validation for the formulation of relatively detailed mathematical models ofin vivolipid peroxidation. Some important aspects of the formulation and analysis of such models are discussed.

ISSN:1071-5762    

DOI:10.3109/10715769509064029

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

The oxidation of low density lipoprotein (LDL) may play an important role in atherosclerosis. We investigated the possible antioxidant effects of mangostin, isolated fromGarcinia mangostana, on metal ion dependent (Cu2+) and independent (aqueous peroxyl radicals) oxidation of human LDL. Mangostin prolonged the lagtime to both metal ion dependent and independent oxidation of LDL in a dose dependent manner over 5 to 50μM as monitored by the formation of conjugated dienes at 234nm (P<0.001). There was no significant effect of mangostin on the rate at which conjugated dienes were formed in the uninhibited phase of oxidation. Levels of thiobarbituric reactive substances (TBARS) generated in LDL were measured 4 and 24 hours after oxidation with 5uM Cu2+in the presence or absence of 50μM or 100μM mangostin. We observed an inhibition of TBARS formation with 100μM mangostin at 4 hours (P = 0.027) but not at 24 hours (P = 0.163). Similar results were observed in the presence of 50μM mangostin. Mangostin, at 100μM, retarded the relative electrophoretic mobility of LDL at both 4 and 24 hours after Cu2+induced oxidation. Mangostin (100μM) significantly inhibited the consumption ofα-tocopherol in the LDL during Cu2+initiated oxidation over a 75 minute period (P<0.001). From these results, we conclude that mangostin is acting as a free radical scavenger to protect the LDL from oxidative damage in thisin vitrosystem.

ISSN:1071-5762    

DOI:10.3109/10715769509064030

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

ISSN:1071-5762    

DOI:10.3109/10715769509064031

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

ISSN:1071-5762    

DOI:10.3109/10715769509064032

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

ISSN:1071-5762    

DOI:10.3109/10715769509064033

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor