• The Korean Journal of Physiology
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• v.5 no.2
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• pp.55-62
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• 1971

In an attempt to better understand the effects of whole body X-irradiation on the levels of non-protein sulfhydryl (NP-SH), non-protein disulfide (NP-SS) and oxygen consumption rate $(QO_2)$ of the mouse duodenum, and to clarify the possible radioprotective action of reduced glutathione (GSH), a whole body X-irradiation of 1,000r was given to albino mouse either singularly or immediately after injecting GSH intraperitoneally to mouse 1 mg per gm of body weight. NP-SH was measured by Ellman's method, NP-SS was measured by the electrolytic reduction method described by Dohan and Woodward, and $(QO_2)$ by the Warburg's standard manometric method. The experiment was performed at 1, 6, 12 and 24 hours post-irradiation, and the comparison was made with the control. The results thus obtained are summarized as follows: 1) Comparing with the intrinsic NP-SH level of $3.31{\pm}0.27{\mu}\;mol/gm$ wet weight in the duodenum of the normal mouse, either whale body X-irradiation or injection of GSH alone produced no significant change in NP-SH from the normal. However, when GSH was injected prior to X-irradiation, markedly elevated NP-SH levels were observed throughout the entire experiment with the highest value of $4.70{\pm}0.10$ at 6 experimental hours. 2) The normal value of NP-SS in the mouse duodenum was $1.57{\pm}0.17{\mu}\;mol/gm$ wet weight, while in the group where injection of GSH and X-irradiation were combined, NP-SS increased to $2.36{\pm}0.33$ at 12 hours and $2.15{\pm}0.53$ at 24 hours, showing the intermediate value between the GSH injection group and X·irradiation group. 3) The normal value of $(QO_2)$ was $4.16{\pm}0.73{\mu}l\;O_2/hr./gm$ D.W., and no noticeable change was observed comparing with the GSH injection group. However, in the group where X·irradiation alone was given, $(QO_2)$ of the duodenum increased significantly throughout the entire experiment with the highest value of $6.35{\pm}1.07$ at 6 experimental hours. When GSH was injected before X-irradiation was given, the levels of $(QO_2)$ were in the middle of the GSH injection group and X-irradiation group. 4) The above results suggest that GSH may be effective as a radioprotector in terms of NP-SH, NP-SS and $(QO_2)$ of the mouse duodenum.

• Journal of Periodontal and Implant Science
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• v.25 no.3
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• pp.529-538
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• 1995

It has been believed that the increased release of free oxygen radicals ($O_2^-,H_2O_2$, and $OH^-$) might be a factor in the pathogenesis of periodontal diseases. Antioxidant enzymes such as glutathione peroxidase(GSH-PX) and catalase can protect the tissue damage from the $H_2O_2$. In order to investigate the GSH-PX and catalase activity in the blood plasma and red blood cells(RBCs) of the patients with periodontitis, 19 patients who had good general health, attachment loss more than 6 mm and bone loss were selected as periodontitis group, 7 patients who had severely inflamed gingiva were selected as gingivitis group, and 15 volunteers with good general and periodontal health were selected as normal group. 17 of 26 patients were performed scaling and root planing to reduce the gingival inflammation for gingivitis and periodontitis groups, and were selected as posttreatment group. After blood plasma and RBCs were collected and separated 1 ml of peripheral blood from each subject, GSH-PX activity in blood plasma and RBCs was measured by the same method that Stefan et al. did, and catalase activity in RBCs was measured by the same method that Beers et al. did. The difference of GSH-PX and catalase activity between normal, gingivitis, and periodontitis groups was statistically analyzed by ANOVA with SPSS/PC+ program, and the difference between pretreatment and posttreatment groups was analyzed by Student t-test. The results were as follows : 1. GSH-PX activity in blood plasma was significantly lower in the gingivitis group($0.8683{\pm}0.0658$), periodontitis group($0.7130{\pm}0.1333$) than in the normal group($1.0241{\pm}0.0801$)(p<0.05), and GSH-PX activity in RBCs was significantly lower in the gingivitis groupt. $0.8156{\pm}0.1167$), periodontitis group($0.7533{\pm}0.1185$) than in the normal group($l.1963{\pm}0.2044$)(P<0.05), but there was no statistical significance in the difference of GSH-PX activity in RBCs between the gingivitis group and periodontitis group(p>0.05). 2. Catalase activity in RBCs was siginficantly lower in the periodontitis group($117.34{\pm}35.01$) than in the normal group($l52.38{\pm}32.09$)(p<0.05). 3. GSH-PX activity in blood plasma was significantly increased in the posttreatment groupe $1.0376{\pm}0.2820$) compared to the pretreatment group(0.7608 0.1600) (p<0.05), and GSH-PX activity in RBC was significantly increased in the posttreatment group($1.0421{\pm}0.2330$) compared to the pretreatment group($0.7728{\pm}0.1210$)(p<0.05). 4. There was no statistical significance in the difference of catalase activity in RBCs between the pretreatment group($112.04{\pm}43.65$) and posttreatment group($l33.41{\pm}39.16$)(p>0.05).The results, within the limits of the present experiment, suggest that the lowered activity of GSH-PX and catalase in blood plasma and RBCs may be related with periodontopathogenesis.

• Biomolecules & Therapeutics
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• v.13 no.4
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• pp.256-262
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• 2005

We examined the signaling molecules involved in the 6-hydroxydopamine (6-OHDA)-induced neuronal cell death and increase in cellular glutathione (GSH) level in SK-N-SH cells. The 6-OH-DA-induced cell death was significantly prevented by the pretreatment with N-acetylcysteine (NAC), a thiol antioxidant, and BAPTA, an intracellular $Ca^{2+}$ chelator. Although 6-OHDA induced ERK phosphorylation, the pretreatment with PD98059, an ERK inhibitor, did not block 6-OHDA-induced cell death. In addition, the 6-OHDA-induced activation of caspase-3, a key signal for apoptosis, was blocked by the pretreatment with NAC and BAPTA. While the level of reactive oxygen species (ROS) was significantly increased in the 6-OHDA-treated cells, the cellular GSH level was not altered for the first 6-hr exposure to 6-OHDA, but after then, the level was significantly increased, which was also blocked by the pretreatment with NAC and BAPTA, but not by PD98059. Depletion of GSH by pretreating the cells with DL-buthionine-(S,R)-sulfoximine (BSO), a glutathione synthesis inhibitor, rather significantly potentiated the 6-OHDA-induced death. In contrast to the pretreatment with NAC, 6-OHDA-induced cell death was not prevented by the post-treatment with NAC 30 min after 6-OHDA treatment. The results indicate that the GSH level which is increased adaptively by the 6-OHDA-induced ROS and intracellular $Ca^{2+}$ is not enough to overcome the death signal mediated through ROS-$Ca^{2+}$ -caspase pathway.

• Nutrition Research and Practice
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• v.16 no.4
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• pp.464-475
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• 2022

BACKGROUND/OBJECTIVES: Increased levels of uremic toxins and decreased antioxidant capacity have a significant impact on the progression of chronic kidney disease (CKD). However, it remains unclear whether they interact with each other to mediate the damage of kidney function. The purpose of this study was to investigate whether uremic toxins (i.e., homocysteine and indoxyl sulfate [IS]), as well as glutathione-dependent antioxidant enzyme activities are dependently or independently associated with kidney function during different stages of CKD patients. SUBJECTS/METHODS: One hundred thirty-two patients diagnosed with CKD at stages 1 to 5 participated in this cross-sectional study. RESULTS: Patients who had reached an advanced CKD stage experienced an increase in plasma uremic toxin levels, along with decreased glutathione peroxidase (GSH-Px) activity. Plasma homocysteine, cysteine, and IS concentrations were all positively associated with each other, but negatively correlated to GSH-Px activity levels after adjusting for potential confounders in all CKD patients. Although plasma homocysteine, cysteine, IS, and GSH-Px levels were significantly associated with kidney function, only plasma IS levels still had a significant association with kidney function after these parameters were simultaneously adjusted. In addition, plasma IS could interact with GSH-Px activity to be associated with kidney function. CONCLUSIONS: IS plays a more dominant role than homocysteine and GSH-Px activity in relation to kidney function.

• 한국생물공학회:학술대회논문집
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• 2003.10a
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• pp.145-148
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• 2003

High concentration of glutathione(GSH) has been found in some species of yeast, of which Saccharomyces cerevisiae is used for commercial fermentative production. In this study, we have investigated the optimal conditions of production which could increase the GSH productivity and used it to maximize the production of GSH in fed-batch culture of Sacchromyces cerevisiae. Fermentation process have been also real time monitored by a 2-dimensional fluorescence sensor.

• Natural Product Sciences
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• v.10 no.4
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• pp.177-181
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• 2004

Antidiabetic treatment with tubers of Asparagus racemosus (Liliaceae) extract (l00 and 250 mg/kg body weight) for three weeks showed significant reduction in thiobarbituric acid reactive substances (TBARS) and glutathione reductase (GSH-R) in both liver and kidney. The treatment with A. racemosus significantly altered the glutathione (GSH) and GSH-R to be comparable with the control group. A. racemosus and glibenclamide treated rats showed decreased lipid peroxidation that is associated with increased activity of superoxide dismutase (SOD) and Catalase (CAT). The ability of A. racemosus on tissue lipid per oxidation and antioxidant status in diabetic animals has not been studied before. The result of this study thus shows that though, A. racemosus possesses moderate antidiabetic activity, but it exhibits potent antioxidant potential in diabetic conditions.

• Proceedings of the Korean Society of Food Science and Nutrition Conference
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• 2004.11a
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• pp.53-60
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• 2004

The pro-apoptotic effect of phenethyl isothiocyanate (PEITC) and the role of glutathione (GSH) in sulforaphane (SFN)-induced antioxidant response element-dependent gene expression were investigated. The caspase-3 and caspase-9 activities were stimulated by PEITC. The release of cytochrome c was time- and dose- dependent. SP600125 suppressed apoptosis induced by PEITC. Similarly, this JNK inhibitor attenuated both cytochrome c release and caspase-3 activation induced by PEITC. SFN is converted to the glutathione conjugate by glutathione S-transferases (GSTs). It was accumulated in mammalian cells by up to several hundred-fold over the extracellular concentration, by conjugation with intracellular GSH. The induction of ARE by SFN was 8.6-fold higher than by SFN-NAC. The decrease in ARE expression at higher concentrations of SFN and SFN-NAC was correlated with the accelerated apoptotic cell death, with a dose-dependent activation of caspase 3 activity by SFN. Upon addition of extracellular GSH within 6 hr of treatment with SFN, the effect on ARE expression was blocked almost completely.

• Journal of Microbiology and Biotechnology
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• v.17 no.9
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• pp.1546-1549
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• 2007

Chitosan oligosaccharide (COS, 3 kDa

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.6
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• pp.1572-1575
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• 2006

Water extract from Cnidii Rhizoma (CRW) was tested for colon cancer chemopreventive activity by measuring the induction of phase II detoxification enzyme activity [quinone reductase (QR) and glutathione S-transferase (GST)] and glutathion (GSH) levels and ornithine decarboxylase (ODC) activity in cultured human colorectal adenocarcinoma HT-29 cells. CRW inhibited cell proliferation in cultured HT-29 cells. CRW induced QR activity in a dose-dependent manner in a concentration range of 0.1${\sim}$5.0 $mg/m{\ell}$. GST activity was also induced with the treatment of CRW in HT-29 cells. In addition GSH levels was increased with CRW. CRW inhibited ODC activity, a key enzyme of polyamine biosynthesis, which is enhanced in tumor promotion. These results suggest that CRW has colon cancer chemopreventive activity by increasing phase II enzyme activity and GSH levels and inhibiting ODC activity in vitro.

• Food Science and Biotechnology
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• v.17 no.6
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• pp.1341-1344
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• 2008

The present study was conducted to investigate the effects of flowers ethanol extract of Elsholtzia splendens (ESE) on the antioxidant defence system in mice with 7,12-dimethylbenz(a)anthracene (DMBA)-induced oxidative stress. The ESE was pre-administered orally to 2 groups of mice at 10 and 50mg/kg body weight (BW) for 5 weeks. Subsequently, mice with pretreatment of ESE received DMBA intragastrically at a dose of 34 mg/kg BW twice a week for 2 weeks. In DMBA alone group, biomarkers of oxidative stress (TBARS value, carbonyl content, and serum 8-OH-dG) were significantly increased. Also, the antioxidant enzymes were down-regulated. ESE significantly restored the TBARS value and carbonyl content at both doses, while a decrease in the elevated serum 8-OH-dG content was observed only at the higher dose. The DMBA-induced decreases in catalase and superoxide dismutase (SOD) activities were restored to nearly control levels by ESE. Glutathione peroxidase (GSH-px) and glutathione reductase (GR) activities, as well as the reduced glutathione (GSH)/oxidized GSH (GSSG) ratio, were significantly affected by ESE at the higher dose. These results suggest that ESE possesses antioxidant activity, which plays a protective role against DMBA-induced oxidative stress.