• Parasites, Hosts and Diseases
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• v.51 no.4
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• pp.479-484
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• 2013

Neutrophils are the predominant inflammatory cells found in vaginal discharges of patients infected with Trichomonas vaginalis. In this study, we examined superoxide anion ($O^{\cdot}_{2^-}$) production by neutrophils activated by T. vaginalis. Human neutrophils produced superoxide anions when stimulated with either a lysate of T. vaginalis, its membrane component (MC), or excretory-secretory product (ESP). To assess the role of trichomonad protease in production of superoxide anions by neutrophils, T. vaginalis lysate, ESP, and MC were each pretreated with a protease inhibitor cocktail before incubation with neutrophils. Superoxide anion production was significantly decreased by this treatment. Trichomonad growth was inhibited by preincubation with supernatants of neutrophils incubated for 3 hr with T. vaginalis lysate. Furthermore, myeloperoxidase (MPO) production by neutrophils was stimulated by live trichomonads. These results indicate that the production of superoxide anions and MPO by neutrophils stimulated with T. vaginalis may be a part of defense mechanisms of neutrophils in trichomoniasis.

• YAKHAK HOEJI
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• v.35 no.3
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• pp.165-173
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• 1991

Effects of eight flavonoids and their related compounds on leukocytes migration, superoxide anion production and lipid peroxidation in the phagocytosis of latex beads or E. coli by guinea pig peritoneal exudate cells were studied in vitro. It shows that most of flavonoids generally inhibited the leukocytes migration and production of superoxide anion and malonedialdehydes. Their inhibitory activities in the phagocytosis of latex beads had more active than that of E. coli. Quercetin has the most inhibitory activity in leukocytes migration and production of superoxide anion and lipid peroxides at the concentration of 1, 2 and 10 $\mu{M}$. Catechin and rutin at the concentration of 2 and 10 $\mu{M}$ inhibited significantly the production of superoxide anion and lipid peroxides. Flavone, catechin, naringin and rutin at the concentration of 2 and 10 $\mu{M}$ inhibited significantly the leukocytes migration.

• Molecules and Cells
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• v.45 no.4
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• pp.193-201
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• 2022

Excessive production of reactive oxygen species (ROS) is a key phenomenon in tumor necrosis factor (TNF)-α-induced cell death. However, the role of ROS in necroptosis remains mostly elusive. In this study, we show that TNF-α induces the mitochondrial accumulation of superoxide anions, not H₂O₂, in cancer cells undergoing necroptosis. TNF-α-induced mitochondrial superoxide anions production is strictly RIP3 expression-dependent. Unexpectedly, TNF-α stimulates NADPH oxidase (NOX), not mitochondrial energy metabolism, to activate superoxide production in the RIP3-positive cancer cells. In parallel, mitochondrial superoxide-metabolizing enzymes, such as manganese-superoxide dismutase (SOD2) and peroxiredoxin III, are not involved in the superoxide accumulation. Mitochondrial-targeted superoxide scavengers and a NOX inhibitor eliminate the accumulated superoxide without affecting TNF-α-induced necroptosis. Therefore, our study provides the first evidence that mitochondrial superoxide accumulation is a consequence of necroptosis.

• Tuberculosis and Respiratory Diseases
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• v.40 no.3
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• pp.223-235
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• 1993

Background: Superoxide anion which was produced by macrophage and neutrophil has a defensive role to kill invasive microorganisms and also an injurious role to produce self lung damage. Production of oxygen free radicals including superoxide is a main mechanism of acute lung injury caused by bacterial endotoxin. Endotoxin is known to activate alveolar macrophage to produce increased oxygen free radicals after the stimulation with various biological materials (priming effect). Calcium is a very important intracellular messenger in that cellular process of superoxide production. Method: This experiment was performed to elucidate the effects of endotoxin and calcium on superoxide production by phorbol myristate acetate-stimulated alveolar macrophage and the effect of verapamil on priming effect of endotoxin. Results: 1) Preincubation of macrophages with endotoxin (E. coli 055-B5) primed the cells to respond with increased superoxide production after the stimulation with PMA. Priming with endotoxin ($10^{-1}$ug/ml) produced a maximal enhancement of superoxide production (43%). 2) Verapamil could inhibit the superoxide production by PMA stimulated macrophage regardless of the presence of extracellular calcium. This means that the inhibitory effect of verapamil is caused by a mechanism independent of blocking calcium influx. 3) Verapamil could inhibit the priming effect of endotoxin on alveolar macrophage (from 30% increment to 13% increment) and could inhibit the superoxide production by PMA-stimulated macrophage preincubated with endotoxin. Conclusion: We concluded that verapamil could inhibit the superoxide production by PMA-stimulated rat alveolar macrophage and also inhibit the priming effect of endotoxin on alveolar macrophage. These inhibitory effects of verapamil could be one of the mechanisms of verapamil effects on endotoxin induced lung injury.

• YAKHAK HOEJI
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• v.52 no.6
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• pp.441-445
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• 2008

To investigate effect of caffeic acid on the intracellular reactive oxygen species production, we used DHE for intracellular superoxide anion production, DCF for intracellular ${H_2}{O_2}$ production and DHR for intracellular hydroperoxide production in Raw 264.7 cells. DPPH assay showed that antioxidant activity of caffeic acid with 39.5 ${\mu}M$ of ${IC}_{50}$ values was similar to that of ascorbic acid with 41.3 ${\mu}M$ of ${IC}_{50}$ values. Caffeic acid dose-dependently inhibited silica-induced ${H_2}{O_2}$ and hydroperoxide production but did not affect superoxide anion production in Raw 264.7 cells, which suggest that antioxidant effect of caffeic acid acts on the post-step of superoxide anion. On the other hand, caffeic acid showed a potent antioxidant effect in $lCuSO_4$-induced lipid peroxidation. Furthermore, plasma superoxide dismutase activity (3.43${\pm}$0.23 U/ml) in 10 mg/kg caffeic acid-fed mice was significantly higher than that (2.32${\pm}$0.24 U/ml) of control. From the above results, it is referred that caffeic acid appears to have potent anti-oxidant activity in both cell system and in vivo system.

• 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.

• Proceedings of the Korean Society for Emotion and Sensibility Conference
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• 2009.05a
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• pp.97-100
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• 2009

The purpose of this study was to examine effects of treadmill running training on superoxide product of spontaneously hypertensive rats. 20 males aged five week old rats were used for the experiments. They were randomly selected into experimental group (10 rats) and control group (10 rats) after being housed in laboratory for two weeks. The rats of experimental group performed treadmill exercise from 15 minutes for the first time to 35 minutes for the last one in order to familiar with experimental protocol ($VO_{2}max\;65{\sim}70%$, 0.9km/h, 5 times/week, 35 minutes/session). They began to perform treadmill running at the age of eight weeks for eight weeks. Superoxide production and NADPH oxidase activities were measured on the aortal from end of experiment. All statistical analyses and description methods were computed by SPSS Version 10.0. Differences in the values between experimental group and control group were calculated using t-tests. The results of this study were: there wewe no significant differences in superoxide production, NADPH oxidase-drivened superoxide activity, NADPH oxidase activity between two groups (p>.05). Spontaneously hypertensive rats of experimental group were characterized by higher superoxide production and lower NADPH oxidase-drivened superoxide activity and NADPH oxidase activity in comparison with the control group. One possible explanation of this finding was that NADPH oxidase activity of experimental group was lower than the control group. It can be concluded that treadmill running for eight weeks was associated positively with superoxide product of spontaneously hypertensive rats.

• Journal of Preventive Medicine and Public Health
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• v.23 no.4 s.32
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• pp.371-390
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• 1990

Production of free radicals of superoxide anion in tissues by cadmium, activities of superoxide dismutase and catalase to protect tissue damages caused by the free radicals and ATPase that plays an important role in energy metabolism at cellular level were investigated. Experiments in vivo were conducted with liver, kidney and testicle tissue homogenates of rats adding $0.05{\sim}0.50mM$ cadmium chloride, and in vivo experiments administering single dose of 5 mg of cadmium/kg of body weight in 0.1% cadmium chloride solution intraperitoneally 48 hours prior to evisceration. Production of superoxide radicals in liver and testicle increased with addition of cadmium in vitro, but not in kidney. In vivo experiments, however, superoxide radicals slightly increased in liver and kidney but not in testicle. Superoxide dismutase (Cu, Zn-SOD and Mn-SOD), catalase and ATPase (total, $Mg^{++}-\;&\;Na^+,\;K^+-$) activity decreased in the presence of cadimium in dose dependent manner. Reduction of these enzyme activities varied not only with dosage of cadmium but also with type of tissue and between in vitro and in vivo experiment.

• Environmental Analysis Health and Toxicology
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• v.8 no.3_4
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• pp.1-5
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• 1993

Using mixed incubation of cultured endothelial cells, cultured fibroblasts, neutrophils activated with PMA and paraquat, the production of superoxide anion, $H_2O$$_2$and lipoxygenase metabolites (5-HETE and 12-HETE) of arachidonate was estimated. The results was as follows: 1. Neutrophils activated with PMA was produced superoxide anion,$H_2O_2$and lipoxygenase metabolites (5-HETE and 12-HETE) of arachidonate. 2. Fibroblasts did not alter the production of superoxide anion and $H_2O_2$ by neutrophils, it was markedly reduced by mixed incubation with endothelial cells. 3. Mixed incubation with endothelial cells significantly augmented the production of 5 or 12-HETEs, but fibroblasts did not. 4. Using mixed incubation of endothelial cells, fibroblasts, neutrophils and paraquat (50ug/m1 and 100ug/m1), the production of superoxide anion, $H_2O_2$and HETEs was significantly increased on both cells at low concentration (50ug/m1), but markedly reduced at high concentration (1001g/m1). 5. Paraquat showed concentration dependent effects on arachidonate lipoxygenase metabolism.

• 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.