• Parasites, Hosts and Diseases
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• v.29 no.3
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• pp.259-266
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• 1991

In cytosolic (raction of adult Paragonimus westermani, superoxide dismutase activity was identified (4.3 units/mg of specific activity) using a xanthine-xanthine oxidase system. The enzyme was purified 150 fold in its activity using the ammonium sulfate precipitation, DEAE-Trisacryl M anion-exchange chromatography and Sephadex G-100 molecular sieve chromatography. The enzyme exhibited the enhanced activity at pH 10.0. The enzyme activity totally disappeared in 1.0mM cyanide while it remained 77.8% even in 10 mM azide. These findings indicated that the ensyme was Cu, Zn-SOD type. Molecular mass of the enzyme was estimated to be 34 kDa by gel filtration and 17 kDa on reducing SDS-polyacrylamide gel electrophoresis which indicated a dimer protein.

• Journal of Microbiology and Biotechnology
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• v.17 no.8
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• pp.1399-1402
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• 2007

The virulence of superoxide dismutase (SOD) mutants of Vibrio vulnificus, as tested by intraperitoneal injection into mice, decreases in the order of sodC mutant, sodA mutant, and sodB mutant lacking CuZnSOD, MnSOD, and FeSOD, respectively. The survival of SOD mutants under superoxide stress also decreases in the same order. The virulence of soxR mutant, which is unable to induce MnSOD in response to superoxide, is similar to that of the sodA mutant, as the survival of the soxR mutant under superoxide stress is similar to that of the sodA mutant. Consistently, the lowered survival of the soxR mutant is complemented not only with soxR but also with sodA. Thus, the virulence of V. vulnificus is significantly affected by the cellular level of SOD activity, and an increase in SOD level through MnSOD induction by SoxR under superoxide stress is essential for virulence.

• Journal of Preventive Medicine and Public Health
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• v.22 no.1 s.25
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• pp.51-56
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• 1989

To investigate the effect of hyperbaric oxygenation on superoxide dismutase activity, neonatal rats (7-10 days old) and adult rats (approximately 100 days old) were continuously exposed to hyperbaric oxygen environment of 2.4ATA for 8 hours and their superoxide dismutase activity were measured. Neonatal rats, all survived through exposure, showed significant increases in the pulmonary superoxide dismutase activity at immediately and 24 hours after exposure. Adult rats, whose 8 hour survival rates were 14%, did not show any significant increase in the activity of pulmonary superoxide dismutase as compared to the control adult rats. These findings are indicating that increased tolerance to oxygen toxicity in neonatal animals during exposure may be attributed to the increase in activity of superoxide dismutase in neonatal rats.

• Korean Journal of Microbiology
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• v.23 no.1
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• pp.69-76
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• 1985

This study was carried out to observe the formation of superoxide radicals and the changes in the activities of superoxide dismutase (EC.1.15.1.1.) from the various organs of a rat which was blocked tricarboxylic acid cycle. In order to block the tricarboxylic acid cycle, the beta-fluoroethylacetate was injected into peritoneal cavity of rat and removed the various tissues from the rat at internals of an hour. By tissue extracts being prepared by the method of Weigiger and Fridovich the activities of superoxide dismutase, aconitase, and contents of bliid glucose, citrates, and wuperoxide radicals were determined. The experimental results are summarized as follows: Accumulation of citrates if increased within three hours after treatment in the all tested tissues, especially, in the geart and spleen they are higher than one of other tissues as 12 and 20 times of control. The activities of aconitase are ingibited to 30-35% on an hour after beta-fluoroethylacetate treatment comparing with that of control rat. The content of blood glucose is increased to 1.6 fold of normal value after 5 hours of treatment. In all tested tissues, superoxide radicals are formed in the heart as 0.26 micromoles per gram tissue between one and three hours after treatment. The activities of total superoxide dismutase are increased between one and three hours after treatment in the all tested tissues and one of these enzymes in heart is highest. The activities of superoxide dismutase containing Mn are also increased with an increase of total superoxide dismutase activities.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.475-483
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• 1994

Background: N-acetylcysteine(ACE) is used both orally and intravenously in a variety of experimental pathologies resembling human disease states which exhibit endothelial toxicity as a result of oxidative stress, including acute pulmonary oxygen toxicity, septicemia and endotoxin shock. Despite these observations in vivo, it is not certain how this thiol drug produces its protective effects. ACE is a cysteine derivative which is able to direct1y react with oxygen radicals and may also act as a cysteine and glutathione(GSH) precursor following deacetylation. In this paper, we tried to know whether the therapeutic doses of ACE can modify the inflammatory function of the neutrophils and can increase the glutathione level of plasma in chronic obstructive pulmonary disease(COPD) patients. In addition, the effect of ACE to the purified neutrophil in terms of superoxide release and glutathione synthesis were observed. Method: Firstly, we gave 600mg of ACE for seven days and compare the release of superoxide, luminol-enhanced chemiluminescence from the neutrophils, neutrophil chemotaxis, and plasma GSH levels before and after ACE treatment in COPD patients. Secondly, we observed the dose dependent effect of ACE to the purified neutrophil's superoxide release and GSH levels in vitro. Results: 1) Usual oral therapeutic doses(600mg per day) of ACE for seven days did affect neither on the neutrophil's superoxide release, chemiluminescence, chemotaxis, nor on the plasma GSH concentration in the COPD patients. 2) ACE decreases the purified neutrophil's superoxide release and increase the GSH production in dose dependent fashion in vitro. Conclusion: Despite the fact that oral ACE treatment did not affect on the neutrophil's inflammatory function and plasma GSH concentration in COPD patients in usual therapeutic doses, it decreases the superoxide release and increases the GSH production from the isolated neutrophils in high molar concentrations. These findings suggest that to obtain an antioxidative effects of ACE, it might be needed to increase the daily dosage of ACE or therapeutic duration or change the route of adminisration in COPD patients.

• The Korean Journal of Pharmacology
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• v.26 no.2
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• pp.145-152
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• 1990

We recently reported a development of an experimental system which can identify the release of a superoxide-dependent vasorelaxant factor from endothelial cells using a two-bath system. In the present work, we further exploited the above system and observed whether the superoxide-dependent relaxing factor(s), released from the porcine coronary artery (PCA) endothelium, was similar in relaxation to those obtained from cat thoracic aortic endothelium and cultured endothelial cells of bovine aorta. However, there was observed a novel difference among the former one and the latter two relaxing factors; the release of relaxing factor from PCA endothelium can be inhibited either by catalase or by superoxide dismutase (SOD), whereas the latter two can be inhibited only by SOD. It was further attempted to characterize the synthetic mechanisms of the relaxing factors: (1) They were readily inhibited by various lipoxygenase inhibitors (gossypol, nordihydroguaiaretic acid, AA 861, and eicosatetraynoic acid). (2) They were not inhibited by cyclooxygenase inhibitor (indomethacin) and by cytochrome P-450 monooxygenease inhibitors (proadifen and cimetidine). Thus, it is likely that these relaxing factors, although obtained from different species, show common functional roles of arteriolar relaxation. It is suggested that they are related to pathophysiological involvement of various tissue ischemia-reperfusion injuries.

• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.123-133
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• 1995

A number of tricyclic antidepressants appear to have inhibitory action on calmodulin. Although amitriptyline, imipramine and doxepine have been shown to inhibit calcium uptake, oxidative phosphorylation and ATPase activities, effects of amitriptyline, imipramine and doxepine on functional responses of human neutrophils have not been elucidated. In this study, effects amitriptyline, imipramine and doxepine on superoxide and hydrogen peroxide generation, myeloperoxidase release, leukocriene B4 formation and intracellular calcium level were investigated. Superoxide and hydrogen peroxide production in heat aggregated IgG-activated neutrophils were inhibited by amitriptyline, imipramine and doxepine. EDTA, EGTA, verapamil and bepredil inhibited heat aggregated IgG-induced superoxide production. Chlorpromazine, trifluoperazine, staurosporine and H-7 also inhibited it. PMA-induced superoxide production was inhibited by amitriptyline, imipramine, doxepine, chlorpromazine and H-7. Amitriptyline, imipramine, chlorpromazine and trifluoperazine inhibited the myeloperoxidase release by heat aggregated IgG. Productions of $LTB_4$, and 5-HETE in heat aggregated IgG-activated neutrophils were inhibited by amitriptyline, imipramine and doxepine. In neutrophils, elevation of intracellular calcium induced by heat aggregated IgG was inhibited by amitriptyline, imipramine, doxepine, chlorpromazine and EGTA, while verapamil slightly inhibited increase of intracellular calcium and H-7 did not inhibit it. These results suggest that the inhibitory effect of amitriptyline, imipramine and doxepine on respiratory burst, myeloperoxidase release and LTB4 production in heat aggregated IgG-activated neutrophils appears to be ascribed to the inhibition of calcium mobilization, calmodulin and protein kinase C.

• Korean Journal of Food Science and Technology
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• v.19 no.6
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• pp.471-474
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• 1987

The formation of superoxide anion (${\cdot}O^{-}_2$)and hydrogen peroxide ($H_2O_2$) during linoleic acid peroxidation were investigated in linoleic acid-aqueous system at $37^{\circ}C$. Superoxide anion was rapidly generated in the early stage of peroxidation, marked to 0.375 (absorbance at 560mm) in the 12mM linoleic acid (POV below 80millieq./kg) incubated for 1 day and then decreased with time-elapsed. Hydrogen peroxide was also rapidly generated in the early stage of peroxidation regardless of linoleic acid concentration. And, superoxide dismutase(SOD) and catalase greatly inhibited the formation of superoxide anion and hydrogen peroxide, respectively.

• Applied Chemistry for Engineering
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• v.20 no.6
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• pp.593-602
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• 2009

For a long time, there is much interest in the superoxide anion radical as one of reactive oxygen species (ROS) not only in the basic research field of chemistry and physics but also in the life science (or biotechnology). Recently, it is becoming ever more vital since the toxic property of nanomaterials as well as advanced oxidation processes (AOP) frequently employed for controlling pollutants are connected with the formation of superoxide anion radicals. Despite many researches on superoxide anion radical, the quantitative information of its presence and its detailed reaction mechanism in aqueous environments remains largely unclear, causing the controversy and confusion. In this review paper, we attempted to summarize the physicochemical property, mechanisms, and applications of superoxide anion radical. In addition, we briefly incorporated the important application of superoxide anion radical in AOP, nanomaterials, and life science (or biotechnology).

• Journal of Photoscience
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• v.4 no.2
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• pp.31-34
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• 1997

The rapid and spontaneous interaction between superoxide anion radical and nitric oxide to yield the potent oxidants. peroxynitrite artion and peroxynitrous acid, was investigated in phorbol myristate acetate(PMA)-stimulated RAW264.7 macrophases by means of lucigenin- or luminol-enhanced chemiluminescence method. When RAW264.7 macrophages were stimulated by PMA. peroxynitrite-induced chemiluminescence was clearly observed. To prove observed chemiluminescencc due to the reaction between superoxide anion radical and nitric oxide produced by RAW264.7 macrophases, N-nitrosoglutathione (GSNO), a nitric oxide-releasing compound. superoxide dismutase(SOD), an enzyme removing superoxide anion radical by dismutating superoxide artion radical to hydrogen peroxide, and N-acethyl cysteine(NAC), a scarvenging reagent both superoxide artion radical and nitric oxide, were added in the cell system. Peroxynitrite- induced chemilumincscence was increased by exogenous addition of GSNO. whereas observed chemiluminescence was decreased by SOD and NAC. These results suggest that PMA-stimulated RAW264.7 macrophages produce both superoxide anion radical and nitric oxide to form peroxynitrite.