• Food Science of Animal Resources
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• v.18 no.2
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• pp.97-106
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• 1998

Antioxidant enzymes such as catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) are known to inhibit oxidative reactions by incativating compounds responsible for the formation of ree radicals. SOD transforms superoxide radical into hydrogen peroxide which is precursor to active free radicals. CAT reduces hydrogen peroxide to water. GSH-Px reduces hydroperoxides to corresponding alcohols. Antioxidant enzyme activities of muscle are different by animal species age, stress and exercise, muscle type and part, conditions of post mortem, storage and processing which are related to oxidative deterioration I muscle foods as well as oxidative defence in living systems. Antioxidant enzyme systems are enhanced rather than weakened in aging skeletal muscle. Red muscle contains higher antioxidant enzyme activity than white muscle. The antioxidant enzyme activities of poultry are higher in leg than in breast, and those of beef are higher in redder and more unstable muscles. It is clear that the effectiveness of the antioxidant enzyme in muscle foods seems to be influenced by meat processing operations. Both GSH-Px and CAT are inactivated by heat processing NaCl also influence the efficiency of the antioxident enzymes since its presence diminishes their catalyitc activity.

• Preventive Nutrition and Food Science
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• v.19 no.4
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• pp.348-352
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• 2014

Black rice contains many biologically active compounds. The aim of this study was to investigate the protective effects of black rice extracts (whole grain extract, WGE and rice bran extract, RBE) on tert-butyl hydroperoxide (TBHP)-induced oxidative injury in HepG2 cells. Cellular reactive oxygen species (ROS), antioxidant enzyme activities, malondialdehyde (MDA) and glutathione (GSH) concentrations were evaluated as biomarkers of cellular oxidative status. Cells pretreated with 50 and $100{\mu}g/mL$ of WGE or RBE were more resistant to oxidative stress in a dose-dependent manner. The highest WGE and BRE concentrations enhanced GSH concentrations and modulated antioxidant enzyme activities (glutathione reductase, glutathione-S-transferase, catalase, and superoxide dismutase) compared to TBHP-treated cells. Cells treated with RBE showed higher protective effect compared to cells treated with WGE against oxidative insult. Black rice extracts attenuated oxidative insult by inhibiting cellular ROS and MDA increase and by modulating antioxidant enzyme activities in HepG2 cells.

• Toxicological Research
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• v.23 no.3
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• pp.207-214
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• 2007

Chronic oxidative stress produced by exposure to environmental chemicals or pathophysiological states can lead animals to aging, carcinogenesis and degenerative diseases. Indirect antioxidative mechanisms, in which natural or synthetic agents are used to coordinately induce the expression of cellular antioxidant capacity, have been shown to protect cells and organisms from oxidative damages. Electrophile and free radical detoxifying enzymes, which were originally identified as the products of genes induced by cancer chemopreventive agents, are members of this protective system. The NFE2 family transcription factor Nrf2 was found to govern expression of these detoxifying enzymes, and screening for Nrf2-regulated genes has identified many gene categories involved in maintaining cellular redox potential and protection from oxidative damage as Nrf2 downstream genes. Further, studies using Nrf2-deficient mice revealed that these mutant mice showed more susceptible phenotypes towards exposure to environmental chemicals/carcinogens and in oxidative stress related disease models. With the finding that cancer chemopreventive efficacy of indirect antioxidants (enzyme inducers) is lost in the absence of Nrf2, a central role of Nrf2 in the antioxidative protective system has been firmly established. Promising results from cancer prevention clinical trials using enzyme inducers propose that pharmacological interventions that modulate Nrf2 can be an effective strategy to protect tissues from oxidative damage.

• YAKHAK HOEJI
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• v.51 no.1
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• pp.75-82
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• 2007

Reactive oxygen species (ROS) are produced in the metabolic process of oxygen in cells. The superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in cells systemize the antioxidant enzymes to control the oxidative stress. Genistein is one of the isoflavonoids, and its role in controlling cellular oxidative stress is presently the active issue at question. In this study; we analyzed genistein-induced survival rates of the CHO-K1 cells, activities of antioxidant enzymes, ROS levels, and expression levels of antioxidant enzyme genes in order to investigate the effect of genistein on cellular ROS production and antioxidative systems in CHO-K1 cells. As results, the survival rate of cells was decreased as the dose of genistein increases (12.5${\sim}$200 ${\mu}$M). Genistein increased cellular ROS levels, while it reduced total SOD activities and the expression of CuZnSOD. In conclusion, we suggest that genistein may induce oxidative stress via down-regulation of SOD.

• Nutritional Sciences
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• v.7 no.1
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• pp.35-40
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• 2004

This study was performed to evaluate the effect of iron supplementation on iron-deficiency-related indices, oxidative stress and antioxidative enzyme activity in female marathoners. Fourteen teenage female marathoners participated in the study. Subjects were divided into two groups: mild anemic and control, depending on their hemoglobin (Hb) level. The mild anemic group had significantly lower RBC count and hematocrit (Hct) and Hb levels compared to the control group. The mild anemic group (〈12.5g Hb/dI, n=7) was given iron supplements (60mg Fe/day) for four weeks during the summer training period. RBC count, Hct and Hb levels showed an increasing tendency through iron supplementation, and significant differences in these variables between the anemic and control groups disappeared in the post-period. There was no difference in plasma malondialdehyde (MDA) between the anemic and control groups. However, catalase (CAT) and glutathione peroxidase (GPx) activity were significantly higher in the anemic group. The significant difference in enzyme activity between the groups disappeared in the post-period. In addition, superoxide dismutase activity significantly decreased after iron supplementation. In conclusion, antioxidative enzyme activity was up-regulated in an anemic condition and mild iron supplementation decreased the antioxidant enzyme activity of female marathoners while improving their anemic condition.

• Biomolecules & Therapeutics
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• v.20 no.5
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• pp.492-498
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• 2012

Phytochemicals have been known to exhibit potent antioxidant activity. This study examined cytoprotective effects of phytochemicals including quercetin, catechin, caffeic acid, and phytic acid against oxidative damage in SK-Hep-1 cells induced by the oxidative and non-oxidative metabolism of ethanol. Exposure of the cells to excess ethanol resulted in a significant increase in cytotoxicity, reactive oxygen species (ROS) production, lipid hydroperoxide (LPO), and antioxidant enzyme activity. Excess ethanol also caused a reduction in mitochondrial membrane potential (MMP) and the quantity of reduced glutathione (GSH). Co-treatment of cells with ethanol and quercetin, catechin, caffeic acid and phytic acid significantly inhibited oxidative ethanol metabolism-induced cytotoxicity by blocking ROS production. When the cells were treated with ethanol after pretreatment of 4-methylpyrazole (4-MP), increased cytotoxicity, ROS production, antioxidant enzyme activity, and loss of MMP were observed. The addition of quercetin, catechin, caffeic acid and phytic acid to these cells showed suppression of non-oxidative ethanol metabolism-induced cytotoxicity, similar to oxidative ethanol metabolism. These results suggest that quercetin, catechin, caffeic acid and phytic acid have protective effects against ethanol metabolism-induced oxidative insult in SK-Hep-1 cells by blocking ROS production and elevating antioxidant potentials.

• Archives of Pharmacal Research
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• v.27 no.8
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• pp.867-872
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• 2004

Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. Mitochondria are especially important in the oxidative stress as ROS have been found to be constantly generated as an endogen threat. Mitochondrial defense depends mainly on super-oxide dismutase (SOD) and glutathione peroxidase (GPx), whereas microsomal defense depends on catalase (CAT), which is an enzyme abundant in microsomes. SOD removes superoxide anions by converting them to $H_2O$$_2$, which can be rapidly converted to water by CAT and GPx. Also, GPx converts hydroperoxide (ROOH) into oxidized-glutathione (GSSG). Ovariectomized (OVX) rats are used as an oxidative stress model. An ovariectomy increased the levels of MDA, one of the end-products in the lipid peroxidative process, and decreased levels of the antioxidative enzymes； SOD, CAT and GPx. However, Chondroitin sulfate (CS) decreased the levels of MDA, but increased the levels of SOD, CAT and GPx in a dose-depen-dent manner. Moreover, inflammation and cirrhosis of liver tissue in CS- treated rats were sig-nificantly decreased. These results suggest that CS might be a potential candidate as an anti oxidative reagent.

• YAKHAK HOEJI
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• v.51 no.4
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• pp.285-290
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• 2007

The oxidative stress causes many diseases like cancer, aging, cardiovascular disease, degenerative neurological disorders (Parkinson’s disease, and Alzheimer's disease) by damage of cell membrane, protein deformation, and damage of DNA due to the oxidation of lipid of cell membrane, protein of tissue or enzyme, carbohydrate, and DNA. It is caused by the reactive oxygen species (ROS) that is produced in the metabolic process of oxygen in cell. The superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in cell systemize the antioxidative enzymes to control the oxidative stress. In this research, it is measured that the survival rate of cell by the typical isoflavonoid of daidzein or genistein, activity of antioxidative enzyme, and ROS level, in order to study the effect of isoflavonoid over the ROS production in cell and antioxidative system. As the similar action of the isoflavonoid with the estrogen is examined, women are encouraged to get bean. In view of this trend, it is very important to find out a combination medicine that lowers the oxidative stress caused by the daidzein in the ovarian cell. In the combined treatment of the typical antioxidant of vitamin C to oxidative stress which induced by daidzein recover the control level particularly lowering the ROS in cell by 30%. However, it made no effect in the combined treatment with genistein. Therefore, the research took the combination effect of daidzein with vitamin C in order to check it effect over the antioxidative system. In conclusion, it was disclosed that the oxidative stress caused by daidzein is related to the lowering activity of SOD, and the specific combination effect of daidzein with vitamin C is related to the recovery of SOD activity.

• BMB Reports
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• v.44 no.5
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• pp.312-316
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• 2011

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its toxic metabolite 1-methyl-4-phenylpyridium ion (MPP$^+$) have been shown to induce Parkinson's disease-like symptoms as well as neurotoxicity in humans and animal species. Recently, we reported that maintenance of redox balance and cellular defense against oxidative damage are primary functions of the novel antioxidant enzyme cytosolic NADP$^+$-dependent isocitrate dehydrogenase (IDPc). In this study, we examined the role of IDPc in cellular defense against MPP$^+$-induced oxidative injury using PC12 cells transfected with IDPc small interfering RNA (siRNA). Our results demonstrate that MPP$^+$-mediated disruption of cellular redox status, oxidative damage to cells, and apoptotic cell death were significantly enhanced by knockdown of IDPc.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.1
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• pp.117-123
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• 2002

This study was Performed to investigate the effect of kimchi intake on antiaging characteristics in the brain of senescence-accelerated mouse (SAM) in terms of free radical production and anti-oxidative enzymes. Two hundreds twenty SAM (20 mice) were divided into four groups and fed kimchi diet for 12 months. Experimental groups were kimchi free AIN-76 diet (control) group, Korean cabbage kimchi diet (KCK)group, 30% mustard leaf added Korean cabbage kimchi diet (MKCK) group, and mustard leaf kimchi diet (MLK) group. Concentrations of total free radical, OH radical and $H_2O_2$ of control group increased up to 123%, 262% and 174% of initial value (p<0.05) after one year. Increase in free radical production in kimchi groups due to aging was decreased by kimchi feeding. Among kimchi groups. MKCK and MLK groups showed greater inhibiting effect against free radical production than KCK. The concentration of TBARS in the bruin of control group also significantly increased up to 362% of initial value as aged (p<0.05) and production of TBARS in kimchi groups were decreased. When the activities of Cu, Zn-SOD, Mn-SOD, GSH-px and catalase of kimchi groups were compared to those of control at the same experimental period, anti-oxidative enzyme activities of kimchi groups were lower than those of control (p<0.05). But GSH/GSSG in kimchi groups were higher compared to control. In conclusion, decrease in free radical production and increase in anti-oxidative enzyme activities were observed from kimchi groups suggesting that kimchi might have important role on retarding aging. Among kimchi variety tested in this experiment, MKCK and MLK seem to have greater effect on inhibiting free radical production and increasing anti-oxidative enzyme activities than KCK.