• Journal of fish pathology
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• v.19 no.3
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• pp.189-195
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• 2006

A subtracted cDNA library of a marine scuticociliate, Philasterides dicentrarchii, in response to 17β-estradiol exposure was constructed using suppression subtractive hybridization (SSH). As a result of SSH, 275 clones were isolated, and among them, only glutathione peroxidase (GPX) gene was isolated as an antioxidative enzyme responding to 17β-estradiol. The semi-quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) analysis revealed that the transcription of GPX gene of P. dicentrarchii was clearly increased by exposure to 17β-estradiol. The GPX transcription was also clearly increased by exposure to xenoestrogens such as bisphenol A (BPA) and genistein.

• Journal of Nutrition and Health
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• v.27 no.9
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• pp.940-948
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• 1994

The present study was designed to determine if prenatal and postnatal Se nutriture affects Se concentration, glutathione peroxidase(GSHPx) activity and phospholipid distribution of the neonatal rat lung. Female SD rats were bred and fed a semipurified Se-deficient(0.04ppm, Se-) or a Se-adequate(0.5ppm, Se+) diet through pregnancy and lactation. On d 2 of lactation, maternal dietary Se had no significant effect on pulmonary Se concentration of pups. On d 16 of lactation, mean milk Se concentration in Se- dams was significantly lower than that in Se+ dams. Milk Se concentration was reflected on lung Se concentration and GSHPx activity of d 16 pups, which were dramatically decreased in Se- pups. In addition, pulmonary disaturated phosphatidyl choline/total phosphatidyl choline ratio was also significantly decreased in Se- pups, implying impaired function of pulmonary surfactant. These data indicate that adequate Se nutrition is important in the maturation of neonatal rat lungs.

• Journal of Nutrition and Health
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• v.20 no.1
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• pp.15-24
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• 1987

To study effects of heated oil on lipid peroxidation in rat liver, rats were fed 3 and 6 weeks by intubating oils heated for l1(HA group) and 24 hours (HB group) at 18$0^{\circ}C$. The contents of lipid peroxides and vitamin E, and the activities of super oxide dismutase and glutathione peroxidase in liver were measured. Histological changes of the liver tissue were observed. In both HA and HE groups, the contents of lipid peroxides and the activities of superoxide dismutase were increased, but the activities of glutathione peroxidase and the contents of vitamin E in liver were decreased when compared to the control group which was fed fresh cora oils. During the oil feeding period, the activities of superoxide dismutase and the contents of vitamin E were not significantly changed, but the activities of glutathione peroxidase were decreased, and lipid peroxides were increased in the 3 weeks than in 6 weeks. In HB liver, the heterochromatin of nucleus increased, mitochondria swellen, cristae in mitochondria disappeared, fat droplet and secondary lysosome increased and lumen of rough endoplasmic reticulum enlarged, compared with that of the control group. These phenomena in HA group were less pronounced.

• Journal of Nutrition and Health
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• v.30 no.7
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• pp.803-812
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• 1997

The influences of dietary supplements of vitamin E on hepatocellular chemical carcinogenesis have been studied, Placental glutathione S-transferase(GST-P) positive foci area, antioxidant enzymes(superoxide dismutase(SOD), catalase, glutathione reductase, glutathione peroxidase, glutathione S-transferase(GST)), glucose 6-phosphatase(G6Pase) activities, and lipid peroxidation of mecrosomes(thiobarbituric acid reactive substances(TBARS) contents) were investigated. For is purpose , we used the murine chemical hepatocardinogenic procedure induced by modified Ito model, which consists of 200mg/kg body weight diethylinitrosamine (DEN) injection, 0.01% 2-acethlaminoflurene(2-AAF) feeding for 6 weeks, and partial hepatectomy on week 3. Weanling Sprague-Dawley male rats were fed pulverized Purina rat chow with 15, 000IU/kg diet vitamin E from initiation or promotion stages. We found that vitamin E supplement decreased the area of GST-P positive foci. Catalase, glutathione peroxidase, glutathione reductase. GST activities, and TBARS contents were decreased. On the other hand G6Pase activities were increased by vitamin E supplement. It seemed that vitamin E supplements helped endogenous defense systems against carcinogenesis by decreasing TBARS contents, $H_2O$$_2$ and organic peroxides. So, vitamin E seemed to protect cell from free radical damage in carcinogenesis. Anticarcinogenic effects of vitamin E were more effective at intiation that at promotion stage. These results suggest that vitamin E has suppressive effects on hepatocellular chemical carcinogenesis, probably through antioxidant effects against TBARS contents $H_2O$$_2$ and orgainc peroxides.

• BMB Reports
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• v.38 no.5
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• pp.563-570
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• 2005

Tamoxifen citrate (TAM), is widely used for treatment of breast cancer. It showed a degree of hepatic carcinogenesis. The purpose of this study was to elucidate the antioxidant capacity of green tea (Camellia sinensis) extract (GTE) against TAM-induced liver injury. A model of liver injury in female rats was done by intraperitoneal injection of TAM in a dose of $45\;mg\;Kg^{-1}\;day^{-1}$, i.p. for 7 successive days. GTE in the concentration of 1.5%, was orally administered 4 days prior and 14 days after TAM-intoxication as a sole source of drinking water. The antioxidant flavonoid; epicatechin (a component of green tea) was not detectable in liver and blood of rats in either normal control or TAM-intoxicated group, however, TAM intoxication resulted in a significant decrease of its level in liver homogenate of tamoxifen-intoxicated rats. The model of TAM-intoxication elicited significant declines in the antioxidant enzymes (glutathione-S-transferase,glutathione peroxidase, superoxide dismutase and catalase) and reduced glutathione concomitant with significant elevations transaminase) levels. The oral administration of 1.5% GTE to TAM-intoxicated rats, produced significant increments in the antioxidant enzymes and reduced glutathione concomitant with significant decrements in TBARS and liver transaminases levels. The data obtained from this study speculated that 1.5% GTE has the capacity to scavenge free radical and can protect against oxidative stress induced by TAM intoxication. Supplementation of GTE could be useful in alleviating tamoxifen-induced liver injury in rats.

• Journal of Ginseng Research
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• v.15 no.2
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• pp.139-143
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• 1991

This study investigated the relations between the photosynthetic rate and the activities of antioxidatile enzymes, glutathione reductase, ascorbate free radical reductase, ascorbate peroxidase, glutathione peroxidase, and ascorbate oxidase, in the leaves of Panax ginseng. Under the normal cultivation condition, Panax in showed lower g1utathione reductase and ascorbate free radical reductase activities the Glycine max. But P ginseng showed higher 91utathione Peroxidase, ascorbate Peroxidase, and ascorbate oxidase activities than C. Panax. Therefore, P. ginseng showed weak activities of reductases for the reduction of the oxidized antioxidants. Under the light intensity of 25 KLux, the reductases showed a decrease of over 75% after 24 hours. But the peroyoxidases decreased about 40%. These results showed that the decrease of reductases acitivities was consistent with the decrease of photosynthetic rate. Therefore, we consider that the regulation of antioxidative enzymes or the application of exogenous antioxidants will be effective means for the protection of photodamage in p. ginseng.

• The Journal of Korean Medicine
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• v.18 no.2
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• pp.355-365
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• 1997

This study was undertaken to examine the effect of Cheongahwan(CAH), being known to reinforce Kidney-yang, on the activities of endogenous antioxidant enzymes and the production of oxygen free radicals in the kidney tissues. Alterations in enzyme activities were observed after in vivo treatment in rats. CAH caused a significant increase in the activities of superoxide dismutase (SOD), glutathione peroxidase and glutathione S-transferase. But catalase activity was not significantly altered by CAH. Treatment in vitro of CAH decreased the production of oxygen free radicals in a dose-dependent fashion. These results suggest that CAH stimulate the activities of antioxidant enzymes and inhibit directly the production of oxygen free radicals. These effects of CAH may contribute to prevent the oxygen free radical-induced impairment of cell function.

• Toxicological Research
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• v.9 no.2
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• pp.159-166
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• 1993

The treatmene of V79 cells with diethyl maleate (DEM) led to decrease in glutathione (GSH) level as increasing DEM concentration. Mercuric chloride, treated for 6 hrs with 2ng/ml, affected the GSH metabolizing enzymes glutathione S-transferase (GST) and glutathione peroxidase (GSP), dropping their activities to 60% and 75%, respectively, though not so much in GSH level(80%). However, the toxic effects of mercuric chloride on those enzymes and GSH level were both amplified when the Hg2+ treatment was combined with the preceding DEM treatment.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.161-161
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• 2001

Phospholipid hydroperoxide glutathione peroxidase (PHGPx) is an antioxidant selenoenzyme which interacts directly with and diminishes peroxidized phospholipids, cholesterol and cholesteryl ester in tissues. PHGPx activity appears in most tissues, but is especially high in testis. In testis, PHGPx level decreases in hypophysectomized rats but is partially restored after gonadotropin treament.(omitted)

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.6
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• pp.678-684
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• 1993

To evaluate the role of xanthine oxidase in liver damage by CCl4, a group of rats were fed tungstate for a month, which suppressed the activities of xanthine oxidase in serum and liver. Control group of rats were fed standard diet without tungstate. Liver damage was induced both in tungstate fed and control groups by two intraperitoneal injections of CCl4 at the level of 0.1ml/100g body weight at intervals of 24 hours. Increases in the levels of serum alanine aminotransferase by CCl4 were significantly smaller in tungstate fed rats than in control rats. Concomitantly, histopathologic changes were less in tungstate fed rats than in control ones. In rats either treated with CCl4 or not, hepatic type O xanthine oxidase activities were remarkably reduced by tungstate feeding. Hepatic aniline hydroxylase activities were higher in rats fed tungstate than control rats when animals were not treated with CCl4, but the enzyme activities were lower in tungstate fed rats than control when they were treated with CCl4. Neither tungstate feeding nor CCl4 treatment caused any significant changes in hepatic glutathione contents, and activities of hepatic glutathione S-transferase, glutathione peroxidase and superoxide dismutase. It is concluded xanthine oxidase reaction augment CCl4 induced liver damage via oxygen free radical system.