• 약학회지
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• 제47권4호
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• pp.218-223
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• 2003

Effect of taurine treatment on metabolism of glutathione (GSH) was studied in adult male ICR mice. An acute injection of taurine (250 mg/kg, ip) resulted in a significant decline of hepatic GSH level at t = 6 hr, but plasma GSH level was not altered. The activity of GSH-related enzyme in liver, such as GSH peroxidase, GSSG reductase, GSH S-transferases, ${\gamma}$-glutamylcysteine synthetase or ${\gamma}$-glutamyltranspeptidase, was not affected by taurine at t = 2.5 or 6 hr. Plasma cysteine and cystine levels were elevated rapidly following taurine treatment. Hepatic cysteine level was decreased by taurine, reaching a level approximately 70％ of control at t = 4 and 6 hr. In conclusion, the results indicate that an acute dose of taurine decreases hepatic GSH level by reducing the availability of cysteine, an essential substrate for synthesis of this tripeptide in liver. It is also suggested that taurine may decrease the cysteine uptake by competing with this S-amino acid for a non-specific amino acid transporter.

• Journal of Ecology and Environment
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• 제29권1호
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• pp.61-67
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• 2006

Tomato (Lycopersicon esculentum Mill) seedlings exposed to various concentrations of $CdCl_2(0{\sim}100{\mu}M)$ in a nutrient solution for up to 9 days were analyzed with respect to the thiol changes and oxidative stress. The Cd exposure increased total non-protein thiols (NPT) and cysteine in both leaves and roots, total glutathione in leaves, and the ratios of oxidized glutathione (GSSG)/reduced glutathione (GSH) in both leaves and roots, but decreased the ratio of dehydroascorbate (DASA)/ascorbate(ASA) in leaves. Our results suggest that the Cd-induced GSH depletion due to thiol synthesis and oxidation alters the antioxidant activity of seedlings for $H_2O_2$, and the subsequent $H_2O_2$ accumulationand oxidative stress result in phytotoxicity.

• 한국동물학회지
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• 제33권4호
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• pp.476-492
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• 1990

흰쥐 간세포에 존재하는 비소결합물질의 특성을 조사하기 위하여 4 ppm의 비소를 포함하는 NaASO$_2$수용액의 식수로 15일간 흰쥐에 공급하였다. 비소처리군의 간 cytosol분획의 정상단백 질의 함량은 감소하였으나 8종류의 stress protein의 함량은 증가하였다. Cytosol에 존재하는 비소결합체물질은 한 종류이고,glycine, glutamic acid 및 cysteine의 3종류의 아미노산으로 구성되어있으며 분자량은 500D이었다.Glutathione은 비소와 5:1의 몰비로 결합하였으며 glutathione과 비소의 복합체는 gel filtration chromatography에서 비소결합물질과 같은 이동성을 나타내어 cytosol에 존재하는 미소결합물질은 glutathione으로 추정되었다. Glutathione에 결합한 비소는 미토콘드리아의 호흡, 형태전환 및 팽윤과 수축기능에 있어서 대조군과 별다른 차이를 나타내지 않았다. 이와 같은 결과들로써, 생체에 직접 처리한 비소에 의하여 stress protein합성이 촉진되며, 간 cytosol에 존재하는 비소결합물질은 glutathione으로 추정되고, 비소와 복합체를 형성함으로써 비소의 세포독성에 대한 방어기능을 나타내는 것으로 생각된다.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
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• pp.166-166
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• 2001

Effects of propargylglycine (PPG) treatment on the hepatic glutathione (GSH) synthesis were examined in adult male ICR mice. Administration of PPG (200 mole/kg, ip) to mice resulted in a complete inhibition of the hepatic cystathionine ${\gamma}$ -lyase (C ${\gamma}$ L) activity measured in cytosol fraction for 40 hr after the treatment. A single injection of PPG rapidly reduced the hepatic GSH levels, which appeared to be sustained at least for 40 hr.(omitted)

• 대한수의학회지
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• 제32권4호
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• pp.629-633
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• 1992

Caffeine이 랫드의 간조직에서 diethylnitrosamine(200mg/kg B.W., DEN)에 의해 유도되는 preneoplastic altered foci형성의 promotion단계에 미치는 효과를 관찰한 바 다음과 같은 결과를 얻었다. Altered foci의 지표로 사용되는 glutathione S-transferase(GST-P)-positive foci의 수는 caffeine 음수 $m{\ell}$당 2mg 병행투여군($3.10{\pm}2.74$) 및 1mg병행 투여군($5.86{\pm}2.83$) 모두에서 DEN 단독투여 대조군($11.55{\pm}5.82$)에 비하여 현저히 낮게 나타났으며 면적 또한 caffeine 2mg 병행투여군($0.13{\pm}0.11$), 1mg 병행투여군($0.21{\pm}0.12$)에서 DEN 단독투여 대조군($0.76{\pm}0.33$)에 비하여 유의성있는 낮은 수치가 관찰되었다. 간 세포배양에서 unscheduled DNA synthesis(UDS)는 DEN($250{\mu}g/m{\ell}$ of medium)단독처리군에 비하여 caffeine($200{\mu}g/m{\ell}$ of medium) 처리시 약 70% 감소하였다. 이러한 결과는 caffeine이 간암발생의 promotion단계에 작용하여 억제효과를 나타냄을 암시하며 이는 DNA회복의 억제와 관계됨을 알 수 있었다.

• 식물조직배양학회지
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• 제22권2호
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• pp.65-70
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• 1995

자리공 모상근에서 betalain의 합성에는 광이 필수이지만 생장률은 암상태 보다 광상태(1500 1X)에서 5배 정도 억제된다. 따라서 광상태에서 모상근의 생장이 억제되는 원인을 규명하기 위해서 항산화제 처리에 따른 효과를 조사하였다. 항산화제(ascorbic acid, glutathione, $\alpha$-tocopherol, sodium pyrosulfate, propylgallic acid) 처리에 따른 모상근의 생장은 암상태에서 무처리보다 1.2-1.4배, 광상태에서 약 1.3-1.9배 생장이 증가되었으며, betalain 합성은 무처리보다 1.2-2.1배 향상되었다. 자리공 모상근의 성장 및 betalain 합성에서 항산화제 복합 처리에 따른 효과는 나타나지 않았다. Betalain 합성 과정에서 항산화제의 효과는 청색 파장하에서 가장 높게 나타났다. 따라서 광상태에서 자리공 모상근의 생장과 betalain 합성을 촉진시키기 위해서는 청색 파장에서 적절한 항산화제의 개발이 요구된다.

• Nutrition Research and Practice
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• 제2권2호
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• pp.80-84
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• 2008

Beneficial effects of dehydroepiandrosterone (DHEA) supplement on age-associated chronic diseases such as cancer, cardiovascular disease, insulin resistance and diabetes, have been reported. However, its mechanism of action in hepatocellular carcinoma in vivo has not been investigated in detail. We have previously shown that during hepatocellular carcinogenesis, DHEA treatment decreases formation of preneoplastic glutathione S-transferase placental form-positive foci in the liver and has antioxidant effects. Here we aimed to determine the mechanism of actions of DHEA, in comparison to vitamin E, in a chemically-induced hepatocellular carcinoma model in rats. Sprague-Dawley rats were administered with control diet without a carcinogen, diets with 1.5% vitamin E, 0.5% DHEA and both of the compounds with a carcinogen for 6 weeks. The doses were previously reported to have anti-cancer effects in animals without known toxicities. With DHEA treatment, cytosolic malate dehydrogenase activities were significantly increased by ${\sim}5$ fold and glucose 6-phosphate dehydrogenase activities were decreased by ${\sim}25%$ compared to carcinogen treated group. Activities of Se-glutathione peroxidase in the cytotol was decreased siguificantly with DHEA treatment, confirming its antioxidative effect. However, liver microsomal cytochrome P-450 content and NADPH-dependent cytochrome P-450 reductase activities were not altered with DHEA treatment. Vitamin E treatment decreased cytosolic Se-glutathione peroxidase activities in accordance with our previous reports. However, vitamin E did not alter glucose 6-phosphate dehydrogenase or malate dehydrogenase activities. Our results suggest that DHEA may have decreased tumor nodule formation and reduced lipid peroxidation as previously reported, possibly by increasing the production of NADPH, a reducing equivalent for NADPH-dependent antioxidant enzymes. DHEA treatment tended to reduce glucose 6-phosphate dehydrogenase activities, which may have resulted in limited supply for de novo synthesis of DNA via inhibiting the hexose monophophaste pathway. Although both DHEA and vitamin E effectively reduced preneoplastic foci in this model, they seemed to fimction in different mechanisms. In conclusion, DHEA may be used to reduce hepatocellular carcinoma growth by targeting NADPH synthesis, cell proliferation and anti-oxidant enzyme activities during tumor growth.

• Biomolecules & Therapeutics
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• 제25권4호
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• pp.427-433
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• 2017

Previously, we demonstrated that galangin (3,5,7-trihydroxyflavone) protects human keratinocytes against ultraviolet B (UVB)-induced oxidative damage. In this study, we investigated the effect of galangin on induction of antioxidant enzymes involved in synthesis of reduced glutathione (GSH), and investigated the associated upstream signaling cascades. By activating nuclear factor-erythroid 2-related factor (Nrf2), galangin treatment significantly increased expression of glutamate-cysteine ligase catalytic subunit (GCLC) and glutathione synthetase (GSS). This activation of Nrf2 depended on extracellular signal-regulated kinases (ERKs) and protein kinase B (AKT) signaling. Inhibition of GSH in galangin-treated cells attenuated the protective effect of galangin against the deleterious effects of UVB. Our results reveal that galangin protects human keratinocytes by activating ERK/AKT-Nrf2, leading to elevated expression of GSH-synthesizing enzymes.

• International Journal of Industrial Entomology and Biomaterials
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• 제6권2호
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• pp.157-162
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• 2003

The glutathione S-transferase (GSTs) are enzymes responsible for the protection of cells from chemical toxicants and oxidative stress. We describe here the cDNA sequence and mRNA expression of a putative GST from the mole cricket, Gryllotalpa orientalis. The G. orientalis GST cDNA sequences comprised of 621 bp encoding 207 amino acid residues. The multiple sequence alignment of G. orientalis GST gene with other known insect GSTs showed several conserved residues that may be essential for the enzymatic activity of the protein. Phylogenetic analysis of the deduced amino acid sequences of G. orientalis GST gene with other insect GST sequences revealed that the G. orientalis GST gene belongs to class I GST, forming a strong monophyletic group (100% bootstrap value) exclusively for class I GSTs from a diverse insect species. Northern blot analysis confirmed midgut-specific expression at transcriptional level, evidencing the midgut as a site for GST synthesis.

• Toxicological Research
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• 제23권2호
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• pp.127-133
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• 2007

Metformin is a drug used to lower blood sugar levels in patients with type 2 diabetes via activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK). The primary objective of this study was to investigate whether metformin at the pharmacologically effective concentrations affects the expressions of ${\gamma}$-glutamylcysteine synthetase and phase II antioxidant genes in the H4IIE cell. Treatment of the cells with either metformin or 5-aminoimidazole-4-carboxamide riboside (AICAR) abrogated tert-butylhydroxyquinone (t-BHQ) induction of ${\gamma}$-glutamylcysteine synthetase, a rate limiting enzyme of GSH synthesis. The ability of t-BHQ to induce glutathione S-transferases (GSTs), a major class of phase II detoxifying enzymes that playa critical role in protecting cells from oxidative stress or electrophiles, was also inhibited by the agents. Transcriptional gene repression by metformin was verified by the GSTA2 promoter luciferase assay. Moreover, either metformin or AICAR treatment significantly decreased t-BHQ-dependent induction of other GSTs (i.e., $GST{\mu}$ and $GST{\pi}$ forms). Taken together, our data indicate that metformin treatment may result in the repression of ${\gamma}$-glutamylcysteine synthetase and glutathione S-transferase genes possibly via AMPK activation.