• Environmental Mutagens and Carcinogens
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• v.25 no.2
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• pp.71-75
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• 2005

Green tea and their major constituents such as catechins are famous materials for their anti-oxidative and anti-carcinogenic activity, but many compounds with reducing power can promote the oxidation in their oxidized form or in the presence of metal ion. We investigated the pro-oxidative effect of the ethanol extract equivalent up to 30mg of dried weight of green tea leaves in four in vitro systems which could be used for detecting DNA damage. Although ethanol extract of green tea did not show significant mutagenicity in Salmonella typhimurium TA102, which is sensitive strain to oxidative stress, it degraded deoxyribose extensively in the presence of $FeCl_3-EDTA$ complex, promoted 8-oxoguanine formation in the live bacteria cell, Salmonella typhimurium TAI04, and cleaved super coiled DNA strand with the help of copper ion. It suggested that green tea, famous anti-oxidative material, can be pro-oxidant according to the condition of extraction or metal existence.

• Biomolecules & Therapeutics
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• v.12 no.3
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• pp.133-137
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• 2004

Present review is built on base of research work on Ganoderma lucidum in our laboratory. A great deal of experimental evidence has suggested that the pharmacological activities of Ganoderma lucidum (Lingzhi) are related to anti-oxidative and free radical scavenging activity. The anti-oxidative and free radical scavenging effects of polysaccharides and triterpenoids isolated from Ganoderma lucidum in different oxidative injury models including tert-butylhydroperoxide (tBOOH)- damaged mice peritoneal macrophages, alloxan-induced diabetes, experimental liver injury models induced by carbon tetrachloride (CCl4), D-galactosamine (DGal) and Bacillus Calmette-Guerin (BCG) plus lipopolysaccharides (LPS) were investigated. It is also demonstrated that Lugu lingzhi, one of Ganoderma product, significantly inhibited LDL oxidation mediated by endothelial cells and decreased monocyte adhesion to endothelial cell (EC) induced by Oxidative low-density lipoprotein (ox-LDL) and advanced glycation endproducts (AGE). Lugulingzhi-treated serum could markedly inhibit the expression of intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-l) induced by ox-LDL and AGE.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2004.04a
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• pp.61-77
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• 2004

Present review is built on base of research work on Ganoderma lucidum in our laboratory. A great deal of experimental evidence has suggested that the pharmacological activities of Ganoderma lucidum(Lingzhi) are related to anti-oxidative and free radical scavenging activity. The anti-oxidative and free radical scavenging effects of polysaccharides and triterpenoids isolated from Ganoderma lucidum in different oxidative injury models including tert-butylhydroperoxide (tBOOH)- damaged mice peritoneal macrophages, alloxan-induced diabetes, experimental liver injury models induced by carbon tetrachloride (CC14), D-galactosamine (DGal) and Bacillus Calmette-Guerin(BCG) plus lipopolysaccharides(LPS) were investigated. It is also demonstrated that Lugu lingzhi, one of Ganoderma product, significantly inhibited LDL oxidation mediated by endothelial cells and decreased monocyte adhesion to endothelial cell (EC) induced by Oxidative low-density lipoprotein (ox-LDL) and advanced glycation endproducts(AGE). Lugulingzhi-treated serum could markedly inhibit the expression of intercellular cell adhesion molecule-l (ICAM-1) and vascular cell adhesion molecule-l (VCAM-1) induced by ox-LDL and AGE.

• Journal of Environmental Health Sciences
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• v.23 no.4
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• pp.9-15
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• 1997

This experiment was carried out to examine the roles of selenium in arsenic- and chromium-induced oxidative stress, which results in chromosomal damage, such as sister chromatid exchange (SCE) and chromosomal aberration (CA). For this purpose, the frequency of CA and SCE related to the level of 0xidative stress were analyzed. Selenium decreased the frequency of CA induced by As. In order to evaluate the effect of selenium on clastogenic factors, media from As- and Cr-treated cells were ultrafiltered and added again to cells in the presence or absence of selenium. Selenium decreased the frequency of SCE by As and Cr. This observation indicates the possibility of presence of clastogenic factor. In addition, the clastogenic factor would be involed in oxidative stress since selenium decreased the level of oxidative stress. Thus, it is suggested that selenium may play a role as an anti-clastogenic effector by preventing the oxidative stress, thereby decreasing the frequency of Asand Cr-induced chromosomal damage.

• The Journal of the Society of Korean Medicine Diagnostics
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• v.17 no.3
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• pp.275-286
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• 2013

In the present study, antioxidant activity and protective effect of extracts from Sambucus williamsii var. coreana stems (SWC) were evaluated on tert-butyl hydroperoxide (t-BHP) induced oxidative stress in human liver (Chang) cells. Antioxidant activities of the SWC extracts were determined by various radical scavenging activities, such as DPPH, ferric reducing antioxidant power (FRAP), 2,2'-azinobis-(3-ethybenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging activity and oxygen radical absorbance capacity (ORAC) assay. SWC extracts showed strong antioxidant effect on various assay. To determine the hepatoprotective effects of SWC on t-BHP induced oxidative damage, cell viability was measured using MTT assay. Pretreatment of SWC extracts showed increasing cell viability, decreasing ROS and restoring mitochondria membrane potential on t-BHP induced oxidative stress in Chang cells. Our findings suggest that SWC extracts may be considered a potential agent for therapeutic protective effect from oxidative stress through its antioxidant activity.

• Journal of Plant Biotechnology
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• v.37 no.4
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• pp.562-566
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• 2010

SOD2-transgenic $T_3$ petunia line (A2-36-2-1-1-35) was treated with different levels of methyl viologen (MV) to determine its resistance to oxidative stress. Four (4) levels of MV (0, 100, 200, and $400\;{\mu}M$) were applied. The SOD2-transgenic $T_3$ petunia line exhibited a very significant oxidative stress resistance at the highest MV concentration ($400\;{\mu}M$) treatment compared to non-transgenic plant. RNA and protein expression of SOD2 transgene and higher parenchyma cell density in the transgenic petunias exhibiting resistance to oxidative stress proves its contribution to the expression of its resistance to oxidative stress.

• Journal of Yeungnam Medical Science
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• v.38 no.2
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• pp.83-94
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• 2021

The global obesity epidemic and the growing elderly population largely contribute to the increasing incidence of type 2 diabetes. Insulin resistance acts as a critical link between the present obesity pandemic and type 2 diabetes. Naturally occurring reactive oxygen species (ROS) regulate intracellular signaling and are kept in balance by the antioxidant system. However, the imbalance between ROS production and antioxidant capacity causes ROS accumulation and induces oxidative stress. Oxidative stress interrupts insulin-mediated intracellular signaling pathways, as supported by studies involving genetic modification of antioxidant enzymes in experimental rodents. In addition, a close association between oxidative stress and insulin resistance has been reported in numerous human studies. However, the controversial results with the use of antioxidants in type 2 diabetes raise the question of whether oxidative stress plays a critical role in insulin resistance. In this review article, we discuss the relevance of oxidative stress to insulin resistance based on genetically modified animal models and human trials.

• Korean Journal of Pharmacognosy
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• v.39 no.4
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• pp.335-340
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• 2008

Diabetes mellitus is metabolic disorder characterized by hyperglycemia caused by insufficient insulin secretion or insulin receptor insensitivity to endogenous insulin. It is well-known that hyperglycemia is one of the main causes of oxidative stress in both type 1 and 2 diabetes. Oxidative stress is related by death of pancreatic ${\beta}$ cell and dysfunction of ${\beta}$ cell. Although ${\beta}$ cell death or dysfunction is induced by many substances or molecules, increased evidences that oxidative stress plays a crucial role in ${\beta}$ cell death or dysfunction. Considering the importance of oxidative stress in the pathogenesis of diabetes mellitus, we investigated the cytoprotective effects against hydrogen peroxide-induced oxidative stress in pancreatic ${\beta}$ cell line RIN-m5F cell. 110 Plant sources were collected in Mt. Baek-du, and extracted with methanol. These extracts had been screened the protective effects against hydrogen peroxide-induced oxidative damage in RIN-m5F cells at 50 and 200 ${\mu}g$/ml. Of these, ten methanolic extracts, aerial part of Erigenron cannadensis, aerial part of Lespedeza juncea, whole plant of Alopecurus aequalis, fruit of Lycium chinense, leaf of Morus alba, rhizome of Polygonatum odoratum, root of Ampelosis japonica, whole plant of Ranunculus japonicus, aerial part of Polygonum sieboldii, rhizome of Arisaema amurense var. violaceum showed significant protective effects against hydrogen peroxide-induced oxidative damage in pancreatic ${\beta}$ cell line RIN-m5F cell.

• Nutrition Research and Practice
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• v.9 no.2
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• pp.123-128
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• 2015

BACKGROUND/OBJECTIVES: Natural products or active components with a protective effect against oxidative stress have attracted significant attention for prevention and treatment of degenerative disease. Oligonol is a low molecular weight polyphenol containing catechin-type monomers and oligomers derived from Litchi chinensis Sonn. We investigated the protective effect and its related mechanism of oligonol against oxidative stress. MATERIALS/METHODS: Oxidative stress in C6 glial cells was induced by hydrogen peroxide ($H_2O_2$) and the protective effects of oligonol on cell viability, nitric oxide (NO) and reactive oxygen species (ROS) synthesis, and mRNA expression related to oxidative stress were determined. RESULTS: Treatment with oligonol inhibited NO and ROS formation under cellular oxidative stress in C6 glial cells. In addition, it recovered cell viability in a dose dependent-manner. Treatment with oligonol also resulted in down-regulated mRNA expression related to oxidative stress, nuclear factor kappa-B (NF-${\kappa}B$) p65, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), compared with the control group treated with $H_2O_2$. In particular, expression of NF-${\kappa}B$ p65, COX-2, and iNOS was effectively reduced to the normal level by treatment with $10{\mu}g/mL$ and $25{\mu}g/mL$ of oligonol. CONCLUSIONS: These results indicate that oligonol has protective activity against oxidative stress-induced inflammation. Oligonol might be a promising agent for treatment of degenerative diseases through inhibition of ROS formation and NF-${\kappa}B$ pathway gene expression.

• The Journal of Natural Sciences
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• v.5 no.2
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• pp.3-11
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• 1992

As concentration of ADP was increased, the rate of phosphocreatine formation by respiring heart mitochondria was increased. The value of apparent Km of the phosphocreatine-forming mitochondria for ADP was estimated to be 0.0185 mM. This value was much lower than that of Km for ATP (0.31 mM) which was determined from the reaction of the soluble form of mitochondrial creatine kinase. The concentration of ATP remained constant during the respiring in the presence of ADP. The rate of accumulation of oxidative-phosphorylated ATP in the mitochondrial respiration medium was continuously monitored as a function of ADP concentration with the firefly luciferase-coupled assay. In that case, exogenous creatine did not affect the rate of accumulation of ATP, indicating that phosphocreatine-forming (i.e.,respiring) mitochondria in the presence of ADP did not use the ATP in the medium as a substrate.These results suggest that the heart mitochondrial creatine kinase bound to the inner membrane functionally tight-coupled to the oxidative phosphorylating system with respect to the respired ATP.