• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.115-122
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• 1995

Effects of staurosporine, genistein and pertussis toxin on superoxide and HOCl production in C5a- or PMA-activated neutrophils were investigated. A C5a-induced superoxide and $H_2O_2$ production was inhibited by staurosporine, genistein and pertussis toxin. The stimulatory effect of PMA was inhibited by staurosporine but was not affected by pertussis toxin, whereas it was further promoted by genistein. Staurosporine and genistein inhibited superoxide production by sodium fluoride, but pertussis toxin did not affect it. PMA-induced $H_2O_2$ production was inhibited by staurosporine but was not affected by pertussis toxin. Genistein did not show a stimulatory effect on PMA-induced $H_2O_2$ production. Staurosporine and pertussis toxin inhibited HOCl production by C5a- or PMA, whereas genistein stimulated it. C5a-or PMA-induced myeloperoxidase release was inhibited by genistein, in this response the effect of pertussis toxin was not detected. Staurosporine did not affect the stimulatory effect of PMA on the release. Myeloperoxidase activity was markedly increased by genistein but was not affected by staurosporine and pertussis toxin. These results indicate that the respiratory burst of neutrophils may be regulated by protein kinase C and protein tyrosine kinase. Superoxide production induced by the direct activation of protein kinase C might be affected by protein tyrosine kinase oppositely. Genistein probably pro-motes HOCl production by activating myeloperoxidase.

• The Korean Journal of Pharmacology
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• v.28 no.2
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• pp.163-170
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• 1992

The present study was attempted to investigate the effect of cyclobuxine (a steroidal alkaloid) on generation of reactive oxygen metablite and myocardial damage promoted by an exogenous administeration of arachidonate in ischemic-reperfused hearts. Langendorff preparation of the isolated rat heart was made ischemic condition by reducing the flow rate to 0.5 ml/min for 45 min, and then followed by normal reperfusion (7 ml/min) for 5 min. The generation of superoxide anion was estimated by measuring the SOD-inhibitable ferricytochrome C reduction. The degree of lipid peroxidation in myocardial tissue was estimated from the tissue malondialdehyde (MDA) concentration using thiobarbituric acid method. The myocardial cell damage was observed by measuring LDH released into the coronary effluent. Sodium arachidonate $(0.1\;and\;1.0\;{\mu}g/ml)$ infused during the period of oxygenated reperfusion stimulated superoxide anion production dose-dependently. The rate of arachidonate-induced superoxide anion generation was markedly inhibited by cyclobuxine $(1.0\;and\;10\;{\mu}g/ml)$. The production of malondialdehyde was increased by infusion of arachidonate. This increase was prevented by superoxide dismutase (300 U/ml) and cyclobuxine $(1.0\;and\;10\;{\mu}g/ml)$. The release of LDH was increased by sodium arachidonate was also inhibited by superoxide dismutase and cyclobuxine. In conclusion, the present results suggest that cyclobuxine inhibits the production of reactive oxygen metabolite and myocardial damages which were promoted by an administeration of arachidonate during reperfusion of ischemic hearts.

• The Korean Journal of Pharmacology
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• v.23 no.2
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• pp.113-121
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• 1987

Local anesthetics were investigated for their effects on mitochondrial electron transport system, production of superoxide radical from submitochondrial particles and malondialdehyde production through lipid per oxidation. Local anesthetics had various effects on activities of enzymes in electron transport chain. The activities of NADH dehydrogenase, NADH oxidase and NADH-ubiquinone oxidoreductase were effectively inhibited by lidocaine, procaine and dibucaine but slightly influenced by cocaine. The activities of succinate dehydrogenase, succinate-cytochrome c oxidoreductase and succinate-ubiquinone oxidoreductase were inhibited by lidocaine and dibucaine, but the succinate oxidase activity was stimulated by local anesthetics. Both dihydroubiquinone-cytochrome c oxidoreductase and cytochrome c oxidase activities were inhibited by local anesthetics. In these reactions, the response of Complex I segment to local anesthetics was greater than other Complex segments. Local anesthetics inhibited both the superoxide production from submitochondrial particles supplemented with succinate or NADH and the enhanced production of superoxide radicals by antimycin. The malondialdehyde production by oxygen free radicals was inhibited by local anesthetics. These results suggest that the inhibition of superoxide and malondialdehyde production caused by local anesthetics may be brought by suppression of the electron transport in mitochondria at sites in or near complex I segment.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.2
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• pp.109-115
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• 2005

Endothelial activation and subsequent recruitment of inflammatory cells are important steps in atherogenesis. The increased levels of cell adhesion molecules (CAM) have been identified in diabetic vasculatures, but the underlying mechanisms remain unclear. To determine the relationship among vascular production of superoxide, expression of CAM and diabetes, superoxide generation and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E- and P-selectin in the aorta from control (C57BL/6J) and diabetic mice (ob/ob) were measured. In situ staining for superoxide using dihydroethidium showed an increased superoxide production in diabetic aorta, accompanied with an enhanced NAD(P)H oxidase activity. Immunohistochemical analysis revealed that the endothelial expression of ICAM-1 ($3.5{\pm}0.4$) and VCAM-1 ($3.8{\pm}0.3$) in diabetic aorta was significantly higher than those in control aorta ($0.9{\pm}0.5$ and $1.6{\pm}0.3$, respectively), accompanied with the enhanced expression of gp91phox, a membrane subunit of NAD(P)H oixdase. Furthermore, there was a strong positive correlation (r=0.89, P＜0.01 in ICAM-1 and r=0.88, P＜0.01 in VCAM-1) between ICAM-1/VCAM-1 expression and vascular production of superoxide. The present data indicate that the increased production of superoxide via NAD(P)H oxidase may explain the enhanced expression of CAM in diabetic vasculatures.

• Microbiology and Biotechnology Letters
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• v.15 no.6
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• pp.381-387
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• 1987

Distribution of superoxide dismutase (SOD) which catalyzes the dismutation of superoxide radicals to hydrogen peroxide and oxygen has been examined in various genera of bacteria. SOD was produced by various bacteria independent of genus and species with variation in superoxide dismutase activity of each bacteria. Bacillus circulans which produced relatively large amount of SOD was selected and used to investigate the optimum culture conditions and further studies. The compositions of optimum culture medium for the enzyme production were 1% glucose, 2% polypeptone, 0.l% NaCl, and 0.2mM of methyl viologen and initial pH was 6.0. The highest enzyme production was observed after 20 hours of cultivation at 3$0^{\circ}C$ on a reciprocal shaker. The enzyme activity was maintained stably for a relatively long period by the addition of 5% ethanol in pH 5.0, 0.01M acetate buffer.

• Applied Biological Chemistry
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• v.43 no.1
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• pp.46-51
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• 2000

The resistance of Cornyza bonariensis to herbicide paraquat was investigated by evaluating the activities of three enzymes concerning in scavenging paraquat-generated toxic oxygen species such as superoxide radical and hydrogen peroxide in resistant and susceptible biotypes. Conyza bonariensis inhabited in cultivated area was more tolerant to paraquat than that of uncultivated area. This is the first report that a biotype of Cornyza bonariensis has appeared in an area with repeated paraquat treatments of Korea. Superoxide dismutase activity of resistant biotype was 20% higher as 150 than that of susceptible biotype. Ascorbate peroxidase activity of resistant biotype was 44% higher than that of susceptible biotype. Glutathione reductase activity of resistant biotype was 64% higher than that of susceptible biotype. It can be concluded from above results that the resistance of Conyza bonariensis to paraquat depends partially on the toxic oxygen species-scavenging efficiency of protective multienzymatic system which is composed of three enzymes, superoxide dismutase, ascorbate peroxidase, and glutathione reductase.

• Korean Journal of Food Science and Technology
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• v.28 no.1
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• pp.184-189
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• 1996

A scavenger of superoxide anion radical which causes oxygen toxicity was isolated from Capsella bursa-pastoris, and its physicochemical properties were investigated. The scavenger was isolated and purified by solvent fractionation and liquid column chromatographies (Amberlite XAD-2, Sephadex LH-20, Bio gel P-2, ODS (silica gel with 100% octadecyl silanization)). An active compound of 0.25 g was finally isolated by Fast Protein Liquid chromatography (FPLC) from 100 g ethanol extract of Capsella bursa-pastoris. A 50% decrease of superoxide anion radical was obtained with the scavenger compound of 0.58 g. The compound was assumed to be a phenolic glycoside from its physicochemical properties.

• Bulletin of the Korean Chemical Society
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• v.28 no.10
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• pp.1881-1884
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• 2007

• Bulletin of the Korean Chemical Society
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• v.29 no.12
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• pp.2399-2402
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• 2008

• Journal of Oral Medicine and Pain
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• v.30 no.3
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• pp.329-336
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• 2005

We examined the effect of PQQ, as a scavenger of superoxide, on osteoclast-like cell formation and on mature osteoclast function. To determine whether PQQ scavenges the superoxide, nitroblue tetrazolium (NBT) staining, which is a method to detect superoxide, was performed on HD-11 cells which are a chick myelomonocytic cell line having tartrate-resistant acid phosphatase (TRAP) activity in response to 1,25-dihydroxyvitamin $D_3\;[1,25(OH)_2D_3]$. Histochemical study of TRAP was also performed on HD-11 cells. PQQ inhibited the TRAP-positive multinucleated cell formation of chicken bone marrow cells was also examined. The addition of 20 ${\mu}M$ PQQ inhibited the formation of TRAP-positive multinucleated cell. When chicken osteoclasts were cultured on dentin slices, treatment of 20 ${\mu}M$ PQQ resulted in a significant decrease in dentin resorption by osteoclasts in terms of total resorption area and number of resorption pits. The present data suggest that PQQ, possibly as a scavenger of superoxide ion, inhibits the osteoclastic differentiation and bone resorption.