• BMB Reports
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• v.33 no.6
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• pp.514-518
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• 2000

Two open reading frames of Haemophilus influenzae, HI0572 and HI0751, showing homology to a yeast thioredoxin peroxidase II (TPx II) and an E. coli thiol peroxidase $P_{20}$, respectively, were cloned and expressed in E. coli, and then the proteins were subsequently purified and characterized. HI0751 protein showed the thioredoxin (Trx)-dependent peroxidase activity, whereas HI0572 protein showed glutathione-dependent peroxidase. The HI0572 is the first peroxiredoxin with glutathione peroxidase activity rather than thioredoxin peroxidase. Purified HI0572 and HI0751 proteins protected specifically the inactivation of glutamine synthetase by metal catalyzed oxidation (MCO) systems composed of $Fe^{3+}$, $O_2$ and mercaptans such as dithiothreitol, ${\beta}-mercaptoethanol$ and glutathione (GSH). Unlike the HI0751 protein, the HI0572 protein was more effective in protecting glutamine synthetase from inactivation by the $GSH/Fe^{3+}/O_2$ system. It seems that these unique properties of the HI0572 protein are due to the structure containing a glutaredoxin domain at it's C-terminal in addition to a peroxiredoxin domain.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.511-519
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• 1998

This study investigated the role of nitric oxide on the oxidative damage in gastric mucosa of rats which received ischemia/reperfusion and its relation to mucus. Nitric oxide synthesis modulators such as L-arginine and $N^G-nitro-L-arginine$ methyl ester, and sodium nitroprusside, a nitric oxide donor, were injected intraperitoneally to the rats 30 min prior to ischemia/reperfusion which was induced by clamping the celiac artery and the superior mesenteric artery for 30 min and reperfusion for 1 h. Lipid peroxide production, the contents of glutathione and mucus, and glutathione peroxidase activities of gastric mucosa were determined. Histological observation of gastric mucosa was performed by using hematoxylin-eosin staining and scanning electron microscopy. The result showed that ischemia/reperfusion increased lipid peroxide production and decreased the contents of glutathione and mucus as well as glutathione peroxidase activities of gastric mucosa. Ischemia/reperfusion induced gastric erosion and gross epithelial disruption of gastric mucosa. Pretreatment of L-arginine, a substrate for nitric oxide synthase, and sodium nitroprusside prevented ischemia/reperfusion-induced alterations of gastric mucosa. However, $N^G-nitro-$ L- arginine methyl ester, a nitric oxide synthase inhibitor, deteriorated oxidative damage induced by ischemia/reperfusion. In conclusion, nitric oxide has an antioxidant defensive role on gastric mucosa by maintaining mucus, glutathione, and glutathione peroxidase of gastric mucosa.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.163-163
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• 2001

Selenium (Se) is an essential micronutrient for mammals and its biological functions are mediated by selenoprotein. In tissues, Se is incorporated into the selenoprotein by recognition of the UGA codon as a stop codon for selenoprotein. Phospholipid hydroperoxide glutathione peroxidase (PHGPx) is an antioxidant selenoprotein that belongs to the superfamily of selenium-dependent peroxidase.(omitted)

• Journal of Ginseng Research
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• v.41 no.3
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• pp.307-315
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• 2017

Background: Red-skin root disease has seriously decreased the quality and production of Panax ginseng (ginseng). Methods: To explore the disease's origin, comparative analysis was performed in different parts of the plant, particularly the epidermis, cortex, and/or fibrous roots of 5-yr-old healthy and diseased red-skin ginseng. The inorganic element composition, phenolic compound concentration, reactive oxidation system, antioxidant concentrations such as ascorbate and glutathione, activities of enzymes related to phenolic metabolism and oxidation, and antioxidative system particularly the ascorbate-glutathione cycle were examined using conventional methods. Results: Aluminum (Al), iron (Fe), magnesium, and phosphorus were increased, whereas manganese was unchanged and calcium was decreased in the epidermis and fibrous root of red-skin ginseng, which also contained higher levels of phenolic compounds, higher activities of the phenolic compound-synthesizing enzyme phenylalanine ammonia-lyase and the phenolic compound oxidation-related enzymes guaiacol peroxidase and polyphenoloxidase. As the substrate of guaiacol peroxidase, higher levels of $H_2O_2$ and correspondingly higher activities of superoxide dismutase and catalase were found in red-skin ginseng. Increased levels of ascorbate and glutathione; increased activities of $\text\tiny L$-galactose 1-dehydrogenase, ascorbate peroxidase, ascorbic acid oxidase, and glutathione reductase; and lower activities of dehydroascorbate reductase, monodehydroascorbate reductase, and glutathione peroxidase were found in red-skin ginseng. Glutathione-S-transferase activity remained constant. Conclusion: Hence, higher element accumulation, particularly Al and Fe, activated multiple enzymes related to accumulation of phenolic compounds and their oxidation. This might contribute to red-skin symptoms in ginseng. It is proposed that antioxidant and antioxidative enzymes, especially those involved in ascorbate-glutathione cycles, are activated to protect against phenolic compound oxidation.

• BMB Reports
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• v.42 no.10
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• pp.648-654
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• 2009

Overexpression of phospholipid hydroperoxide glutathione peroxidase (PHGPx) genes has been reported to play an important role in protecting host cells from oxidative injury in several model systems. A radish phospholipid hydroperoxide glutathione peroxidase (RsPHGPx) known to have high catalytic activity was applied to mouse 3T3 fibroblasts to determine the protective effects of PHGPx against oxidative injury triggered by hydroperoxides such as hydrogen peroxide ($H_2O_2$), tert-butyl hydroperoxide (t-BHP) and phosphatidylcholine hydroperoxide (PCOOH). We observed that preincubation of cells with RsPHGPx significantly increased cell viability, reduced levels of malondialdehyde (MDA), inhibited generation of reactive oxygen species (ROS), and maintained natural cell shapes after treatment with $H_2O_2$, t-BHP or PCOOH, indicating that the exogenous RsPHGPx can act as an effective hydroperoxide-scavenger and may also protect target cells from oxidative damage. These results suggest the possibility for use of RsPHGPx as a therapeutic protectant.

• Journal of Nutrition and Health
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• v.33 no.7
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• pp.733-738
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• 2000

The purpose of this study was to investigate the effects of green tea on gene expression of superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px) in rat liver exposed to microwave. Sprague-Dawley male rats with 200$\pm$10g body weight were assigned to normal and microwave exposed groups : microwave exposed groups ; microwave exposed groups were divided two groups : microwave(MW) group which was administrated the distilled water and green tea(GT) group which was administrated the green tea extracts. The rats were irradiated with microwave at frequence of 2.45 GHz for 15 min and then the gene expression in the damaged tissue were investigated at 0.1, 3, 4,6 and 8 days after the microwave irradition to compared with the normal group. The level of SOD gene expression in MW group was lower than the normal group within 6 days but that of GT group as higher than MW group. These results may imply that green tea stimulates SOD expression and there by protecting tissues from free radicals. The GSH-Px gene was expressed a little bit lower than the normal group but that of GT group was expressed to higher lever than MW group from 4 days after irradiation. These results suggest that the administration of green tea extract may activate antioxidative gene expressions such as SOD and GSH-Px in rat and that may help to recover liver tissues from microwave damage by removing hazardous free radicals and oxidized by products from cells.

• Journal of Nutrition and Health
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• v.44 no.2
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• pp.112-118
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• 2011

We investigated the selenium (Se) nutrition status in Korean infants. The mean serum Se concentration in infants was 66.9 ${\mu}g/L$, and it increased with increasing in infant age: 57.6 ${\mu}g/L$ at 0-5 months, 71.8 ${\mu}g/L$ at 6-11 months, and 75.5 ${\mu}g/L$ at 12-24 months. Serum glutathione peroxidase (GPx) activity also increased with infant age. Serum Se concentration in infants was positively correlated with serum GPx activity (r = 0.565, p < 0.01). At 0-5 months, human milk-fed infants tended to have higher Se concentrations and GPx activity than those of formula-fed infants, but the result was not significant. With the introduction of supplemental feeding at 6-24 months of age, serum Se concentration was not different between the groups. Therefore, human milk feeding seemed to be more appropriate for infant Se nutrition than infant formula feeding during the first 6 months of life, but supplemental feeding became more important later to maintain good Se nutrition status.

• Molecules and Cells
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• v.21 no.2
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• pp.276-283
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• 2006

The potent environmental contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), induces thymus atrophy in experimental animals. However, its mechanism of action is not fully understood. To gain insight into its immunosuppressive effect, Balb/c mice were intraperitoneally injected with TCDD ($30{\mu}g/kg$ body weight) and genes regulated by TCDD were identified using cDNA arrays [Park and Lee (2002)]. One of the regulated genes was that for plasma glutathione peroxidase (pGPx). Upon TCDD injection, pGPx mRNA levels in the thymus increased, in parallel with increases in GPx activity and the frequency of anti-human pGPx antibody-reactive cells. pGPX mRNA levels were also moderately up-regulated in the testis and spleen. This is the first report that a particular isotype of the glutathione peroxidase family is regulated by TCDD at both mRNA and protein levels. pGPx is expressed in various tissues in contact with body fluids, and detoxifies hydrogen peroxides and lipid hydroperoxides. It will be of interest to assess the role of pGPx in TCDD-induced thymic atrophy.

• Journal of Nutrition and Health
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• v.29 no.7
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• pp.721-728
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• 1996

The level of oxidative tissue damage caused by free radicals generated from ethanol oxidation was determined in the myocardium of chronic ethanol fed-rats and the protective action of various radical scavenging enzymes was monitored, also. Adult male Sprague-Dawley rats were given ethanol in an amount of 36% of total calories via Lieber-DeCarli liquid diet for 6 weeks. Control group was pair-fed with the diet containing isocaloric amount of dextrin-maltose instead of ethanol. Chronic ethanol administration resulted in the increased amount of myocardial thiobarbituric acid reactive substance(TBARS), th parameter of lipid peroxidation, under our experimental condition. Chronic ethanol ingestion did not cause any change in activities of either glutathione peroxidase or glutathione reductase and glucose-6-phosphate dehydrogenase were decreased after ethanol treatment. Therefore, chronic ethanol administration seemed to cause considerble changes in cellular defense function against oxidative tissue damage in rat myocardium through glutathione utilizing system and radical generation system. However the ultimate net result of chronic ethanol inestion on the myocardium of rat was the oxidative tissue damage revealed by increased TBARS content.

• BMB Reports
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• v.38 no.3
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• pp.300-306
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• 2005

Tamoxifen citrate is an anti-estrogenic drug used for the treatment of breast cancer. It showed a degree of hepatic carcinogenesis, when it used for long term as it can decrease the hexose monophosphate shunt and thereby increasing the incidence of oxidative stress in liver rat cells leading to liver injury. In this study, a model of liver injury in female rats was done by intraperitoneal injection of tamoxifen in a dose of 45 mg/kg body weight for 7 successive days. This model produced a state of oxidative stress accompanied with liver injury as noticed by significant declines in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant elevations in TBARS (thiobarbituric acid reactive substance) and liver transaminases; sGPT (serum glutamate pyruvate transaminase) and sGOT (serum glutamate oxaloacetate transaminase) levels. The oral administration of dimethyl dimethoxy biphenyl dicarboxylate (DDB) in a dose of 200 mg/kg body weight daily for 10 successive days, resulted in alleviation of the oxidative stress status of tamoxifen-intoxicated liver injury in rats as observed by significant increments in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant decrements in TBARS and liver transaminases; sGPT and sGOT levels. The administration of DDB before tamoxifen intoxication (as protection) is more little effective than its curative effect against tamoxifen-induced liver injury. The data obtained from this study speculated that DDB can mediate its biochemical effects through the enhancement of the antioxidant enzyme activities and reduced glutathione level as well as decreasing lipid peroxides.