• Journal of Plant Biotechnology
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• v.33 no.1
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• pp.1-9
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• 2006

Peroxiredoxins (Prxs) are ubiquitously distributed and play important functions in diverse cellular signaling systems. The proteins are largely classified into three groups, such as typical 2-Cys Prx, atypical 2-Cys Prx, and 1-Cys Prx, that are distinguished by their catalytic mechanisms and number of Cys residues. From the three classes of Prxs, the typical 2-Cys Prx containing the two-conserved Cys residues at its N-terminus and C-terminus catalyzes $H_2O_2$ with the use of thioredoxin (Trx) as an electron donor. During the catalytic cycle, the N-terminal Cys residue undergoes a peroxide-dependent oxidation to sulfenic acid, which can be further oxidized to sulfinic acid at the presence of high concentrations of $H_2O_2$ and a Trx system containing Trx, Trx reductase, and NADPH. The sulfinic acid form of 2-Cys Prx is reduced by the action of sulfiredoxin which requires ATP as an energy source. Under the strong oxidative or heat shock stress conditions, 2-Cys Prx in eukaryotes rapidly switches its protein structure from low-molecular-weight species to high-molecular-weight protein structures. In accordance with its structural changes, the protein concomitantly triggers functional switching from a peroxidase to a molecular chaperone, which can protect its substrate denaturation from external stress. In addition to its N-terminal active site, the C-terminal domain including 'YF-motif' of 2-Cys Prx plays a critical role in the structural changes. Therefore, the C-terminal truncated 2-Cys Prxs are not able to regulate their protein structures and highly resistant to $H_2O_2$-dependent hyperoxidation, suggesting that the reaction is guided by the peroxidatic Cys residue. Based on the results, it may be concluded that the peroxidatic Cys of 2-Cys Prx acts as an '$H_2O_2$-sensor' in the cells. The oxidative stress-dependent regulation of 2-Cys Prx provides a means of defense systems in cells to adapt stress conditions by activating intracellular defense signaling pathways. Particularly, 2-Cys Prxs in plants are localized in chloroplasts with a dynamic protein structure. The protein undergoes conformational changes again oxidative stress. Depending on a redox-potential of the chloroplasts, the plant 2-Cys Prx forms super-molecular weight protein structures, which attach to the thylakoid membranes in a reversible manner.

• Korean Journal of Plant Resources
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• v.18 no.3
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• pp.470-478
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• 2005

The objective of present study was to investigate the hepatoprotective and antioxidative effects of onion extracts. Primary cultures of rat hepatocytes were incubated with 1.5 mM tort-butyl hydroperoxide(t-BHP), potent oxidizing agent to liver, for 1 hr in the presence or absence of various concentrations (0, 0.01, 0.05, 0.1 or 0.3 mg/ml) of onion extract. Incubation with t-BHP increased glutamic oxaloacetic transaminase(GOT) and lactate dehydrogenase(LDH) acitivities and thiobarbituric acid reactive substances(TBARS) concentration but decreased 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT) reduction. Onion extracts at the concentration of 0.05 mg/ml decreased t-BHP-induced GOT and LDH activities. Onion extract at the concentration of 0.1 mg/ml increased t-BHP-induced MTT reduction. Onion extract at the concentration of 0.01 mg/ml decreased t-BHP-induced TBARS concentration. Taken together, onion extracts prevented t-BHP-induced hepatocyte injury and lipid peroxidation. Catalase, glutathione peroxidase(GSH-Px) and glutathione reductase(GSH-Rd) activities of hepatocytes were significantly decreased by t-BHP. Onion extracts at the concentration of 0.1 mg/ml prevented t-BHP-induced decrease in catalase, GSH-Px and GSH-Rd activities. Onion extracts prevented hydroxyl radical-induced single-strand breakage in dose-dependent manner when plasmid DNA was incubated with various concentrations of onion extracts in the presence of Fenton reagents producing hydroxyl radical. These results demonstrate that onion extracts suppressed t-BHP-induced cytoctoxicity, decreased viability and lipid peroxidation and increased GSH-Px, GSH-Rd and catalase activities. Thus hepatoprotective and antioxidant effects of onion extract seem to be due to, at least in part, the increase in antioxidant enzyme activities as well as prevention from hydroxyl radical-induced oxidation, followed by inhibition of lipid peroxidation.

• Journal of the Korean Society of Food Science and Nutrition
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• v.24 no.2
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• pp.183-194
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• 1995

The purpose of this study was to investigate the effect of vitamin E on the synthesis of the metallothionein in the liver of streptozotocin (STZ)-induced diabetic rats. Sprague-Dawley male rats($220{\pm}10mg$) were randomly assigned to one control and three STZ-diabetic groups. Diabetic groups were classified to STZ-0E(vitamine E free diet), STZ-40E(40mg vitamin E/kg of diet) and STZ-400E(400mg vitamin E/kg of diet) according to the level of vitamin E supplementation. Blood glucose levels of STZ-diabetic rats were three times higher than that of control. The contents of vitamin E in liver were lower signifciantly STZ-0E, STZ-40E groups by 50%, 36% compared with that of control. Lipid peroxide values(LPO) in liver were higher 5.6 and 2.5 times in STZ-0E and STZ-40E groups than that of control. Plasma cortisol levels were higher STZ-0E and STZ-40E groups compared with those of control, but cortisol levels were lower significantly in STZ-400E group compared with those of the STZ-0E and the STZ-40E groups. The plasma insulin levels were lower in all three STZ-diabetic group compared with that of control, but were not affected by the level of dietary vitamin E. The metallothionein (MT) contents in liver, kidney and small intestine were five times higher in STZ-0E, STZ-40E and STZ-400E compared with that of control, but STZ-400E group was lower in the MT contents in tissues compared with that of STZ-40E group. Zn-MT peak in STZ-diabetic rats liver increased than that of control by Sephadex G-75, and Zn-MT peak divided into MTI and MTII peaks by DEAE Sephadex A-25 column chromatography. The present results indicate that STZ-induced diabetic rats are more sensitive to oxidative stress, leading to the acceleration of lipid peroxidation process, which can be more promoted low level of dietary vitamin E. And the result may that increase synthesis of MT induced in the liver of diabetic rats increased so it can be sure that the diabetes is one of the MT induce factor by free radical generation. And high vitamin E supplementation reduced total MT contents of liver, kidney and small intestine and the peak of purified Zn-MT. Through the results of these experiments, we can conclude that MT might be the free radical scavenger.

• Journal of the Korean Society of Food Science and Nutrition
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• v.30 no.6
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• pp.1260-1265
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• 2001

This study was performed to investigate the protective effects of Hovenia dulcis Thunb on hepatotoxicity in carbon tetrachloride-intoxicated rats. Male Sprague-Dawley rats (220~240 g) were used as experimental groups, which were divided into 7 groups; Control group, $CCl_4$-treated group, hexane fraction pretreated and $CCl_4$-treated group, chloroform fraction pretreated and $CCl_4$-treated group, ethylacetate fraction pretreated and $CCl_4$-treated group, butanol fraction pretreated and $CCl_4$-treated group, $H_2O$ fraction pretreated and $CCl_4$-treated group. After 6 days, the activities of aminotransferase, contents of cholesterol, TG and hepatic lipid peroxide content in chloroform fraction pretreated and $CCl_4$-treated group were significantly decreased (p<0.05) compared to the only $CCl_4$-treated group. The content of glutathione and activities of GST in chloroform fraction pretreated and $CCl_4$-treated group were also significantly increased (p<0.05) compared to the only $CCl_4$-treated group. In addition, activities of SOD, catalase and GSH-Px in chloroform fraction pretreated and $CCl_4$-treated group were significantly decreased (p<0.05) compared to the only $CCl_4$-treated group. These results indicated that the chloroform fraction of Hovenia dulcis Thunb methanol extract showed hepatoprotective effect in carbon tetrachloride-intoxicated rats.

• Journal of the Korean Society of Food Science and Nutrition
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• v.38 no.6
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• pp.683-693
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• 2009

This study was designed to investigate the effect of dandelion juice supplementation on attenuation of oxidative stress and hangover after drinking alcohol in healthy college male students. This human trial was conducted by two phase cross over design with two weeks wash out period. The subjects (age $24{\sim}28$ years) were volunteers who had more than 72 g of ethanol drinking capacity. Dandelion group was given dandelion juice 220 mL daily for 7 days. Biochemical markers were determined in blood samples taken at 0 and 150 minutes after administration 72 g of alcohol. The levels of plasma glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, lactate dehydrogenase and bilirubin, the indicators of liver cell damage, were not significantly different between groups. No significant differences in lymphocyte DNA damage level between groups was observed. However, plasma acetaldehyde dehydrogenase (ALDH) and high density lipoprotein cholesterol levels were significantly (p<0.01) increased in dandelion supplemented group compared to that of control group. Furthermore, activities and protein expressions of glutathione-reductase and catalase of erythrocytes were significantly elevated in dandelion supplemented group compared to that of control group. From the above results, it is concluded that dandelion juice supplementation can reduce oxidative stress and hangover syndrome through the elevation of ALDH and antioxidative enzyme system in healthy male adults.

• Korean Journal of Food Science and Technology
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• v.49 no.6
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• pp.649-658
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• 2017

The potential of the ethyl acetate fraction from Pteridium aquilinum (EFPA) to improve the cognitive function in high-fat diet (HFD)-induced diabetic mice was investigated. EFPA-treatment resulted in a significant improvement in the spatial, learning, and memory abilities compared to the HFD group in behavioral tests, including the Y-maze, passive avoidance, and Morris water maze. The diabetic symptoms of the EFPA-treated groups, such as fasting glucose and glucose tolerance, were alleviated. The administration of EFPA reduced the acetylcholinesterase (AChE) activity and malondialdehyde (MDA) content in mice brains, but increased the acetylcholine (ACh) and superoxide dismutase (SOD) levels. Finally, kaempferol-3-o-glucoside, a major physiological component of EFPA, was identified by using high-performance liquid chromatography coupled with a hybrid triple quadrupole-linear ion trap mass spectrometer (QTRAP LC-MS/MS).

• Journal of Nutrition and Health
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• v.48 no.2
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• pp.140-148
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• 2015

Purpose: The purpose of this study was to evaluate the role of coffee in diabetic rats in order to prevent hyperglycemia and hyperlipidemia, and to improve antioxidant enzyme activity in streptozotocin induced diabetic rats. Methods: Thirty two male Sprague-Dawley rats (body weight $200{\pm}5g$) were divided into two groups; diabetic and nondiabetic groups. The groups were each randomly divided into two subgroups; fed control and coffee (5 g coffee powder/kg diet) diets. Diabetes was induced by intramuscular injection of 50 mg streptozotocin/kg body weight. Rats with blood glucose concentrations ${\geq}300mg/dL$ were considered diabetic for these experiments. All rats were fed an experimental diet and deionized water ad libitum for 4 weeks. Results: The results of this study indicate that body weight gain was significantly lower in diabetic groups than in nondiabetic groups regardless of diet. Mean food intake was significantly higher in diabetic groups than in nondiabetic groups, and significantly higher in the coffee group than in the control group in diabetic rats. Food efficiency ratio (FER) was significantly lower in diabetic groups than in nondiabetic groups regardless of diet. The fasting blood glucose of coffee supplemented groups was significantly lower compared with the control group in diabetic and nondiabetic rats. The levels of serum LDL-cholesterol and atherogenic index were significantly lower in the coffee group than in the control group in diabetic and nondiabetic rats, and serum HDL-cholesterol was significantly higher in the coffee group than in control groups. The contents of hepatic triglyceride were significantly lower in the coffee group than in the control group in diabetic and nondiabetic rats. The lipid peroxidation of malondialdehyde (MDA) contents was significantly lower in the coffee group than in the control group in diabetic and nondiabetic rats. Activity of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase in liver was not significantly different by experimental diets among all groups. Conclusion: In conclusion, effects of 0.5% coffee powder supplemented diet were beneficial on blood glucose and lipids in diabetic rats.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.10
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• pp.1164-1170
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• 2017

Protaetia brevitarsis larvae (PBL) has recently been registered as a temporary food in Korea, and this study evaluated the application potential of PBL proteins as health functional food materials. Protein hydrolysates were prepared from PBL powder by enzymatic hydrolysis using five different proteases (alcalase, bromelain, flavourzyme, neutrase, and papain), and based on the results from the peptide content and SDS-PAGE analyses, PBL treated with alcalase or flavourzyme showed a high degree of hydrolysis (HD) value, whereas the HD value of those treated with neutrase, bromelain, or papain was minimal. The protein hydrolysates showing a high HD value were separated further into the fractions of >3 kDa and <3 kDa by a centrifugal filter system and then lyophilized, and according to the $RC_{50}$ values of the protein hydrolysates (<3 kDa) obtained from three different antioxidant analyses; the alcalase hydrolysates showed the highest antioxidant activity. Therefore, the alcalase hydrolysates were tested further for their inhibitory effects on the peroxidation of linoleic acid by measuring the thiobarbituric acid values. The results showed that the peroxidation of untreated linoleic acid increased dramatically during 6 days of incubation, but a pretreatment with the hydrolysates ($100{\sim}800{\mu}g/mL$) significantly inhibited the linoleic acid peroxidation in a dose-dependent manner for 6 days. Our current studies are focused on the identification of active peptide sequences from alcalase hydrolysates.

• Tuberculosis and Respiratory Diseases
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• v.41 no.3
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• pp.222-230
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• 1994

Background: Paraquat, a widely used herbicide, is extremely toxic, causing multiple organ failure in humans. Paraquat especially leads to irreversible progressive pulmonary fibrosis, which is related to oxygen free radicals. However, its biochemical mechanism is not clear. Natural mechanisms that prevent damage from oxygen free radicals include changes in glutathione level, G6PDH, superoxide dismutase(SOD), catalase, and glutathione peroxidase. The authors think catalase is closely related to paraquat toxicity in the lungs Method: The effects of 3-amino-1,2,4-triazole(aminotriazole), a catalase inhibitor, on mice administered with paraquat were investigated. We studied the effects of aminotriazole on the survival of mice administered with paraquat, by comparing life spans between the group to which paraquat had been administered and the group to which a combination of paraquat and aminotriazole had been administered. We measured glutathion level, glucose 6-phosphate dehydrogenase(G6PDH), superoxide dismutase(SOD), catalase, and glutathione peroxidase(GPx) in the lung tissue of 4 groups of mice: the control group, group A(aminotriazole injected), group B(paraquat administered), group C(paraquat and aminotriazole administered). Results: The mortality of mice administered with paraquat which were treated with aminotriazole was significantly increased compared with those of mice not treated with aminotriazole. Glutathione level in group B was decreased by 20%, a significant decrease compared with the control group. However, this level was not changed by the administration of aminotriazole(group C). The activity of G6PDH in all groups was not significantly changed compared with the control group. The activities of SOD, catalase, and glutathione peroxidase(GPx) in the lung tissue were significantly decreased by paraquat administration(group B); catalase showed the largest decrease. Catalase and GPX were significantly decreased by aminotriazole treatment in mice administered with paraquat but change in SOD activity was not significant(group C). Conclusion: Decrease in catalase activity by paraquat suggests that paraquat toxicity in the lungs is closely related to catalase activity. Paraquat toxicity in mice is enhanced by aminotriazole administration, and its result is related to the decrease of catalase activity rather than glutathione level in the lungs. Production of hydroxyl radicals, the most reactive oxygen metabolite, is accelerated due to increased hydrogen peroxide by catalase inhibition and the lung damage probably results from nonspecific tissue injury of hydroxyl radicals.

• Journal of Life Science
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• v.26 no.2
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• pp.226-233
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• 2016

Vascular smooth muscle cell (VSMC) apoptosis has been identified in various vascular diseases, including atherosclerosis and restenosis after angioplasty, and has been known to precipitate atherosclerotic plaque instability and rupture. Oxysterols are known as inducers of apoptosis in VSMC, and 7-ketocholesterol (7KC) is the major nonenzymically formed oxysterol in atherosclerotic lesions. The precise mechanism underlying VSMC apoptosis is still poorly understood. In this study, we investigated whether 7KC causes apoptosis, and characterized its apoptotic mechanisms in primary cultured rat aortic VSMC. Cell viability was assessed by MTT assay and trypan blue assay. Apoptosis was assessed by flow cytometry, immunofluorescence, immunoprecipitation, and Western blot analyses. 7KC markedly decreased the VSMC viability in a time- and concentration-dependent manner, and increased the production of 4-hydroxynonenal (HNE), a major end-product of lipid peroxidation, which also decreased the VSMC viability. Pretreatment with 2,4-dinitrophenylhydrazine, a well-known reagent of lipid peroxidation-derived aldehydes, significantly restored the 7KC-decreased viability of VSMC. Furthermore, HNE, as well as 7KC, reduced the level of total Akt, a major mediator of cell survival. The 7KC-decreased level of total Akt was significantly restored by pretreatments with 2,4-dinitrophenylhydrazine and N-acetylcysteine. Lactacystin, a proteasome inhibitor, protected VSMC against apoptosis and Akt degradation, but did not inhibit HNE production. In the immunoprecipitation assay, 7KC increased HNE-modified Akt. From the results, it seems that, in atherosclerotic lesions, 7KC induces HNE production in VSMC, and this HNE binds to Akt, proceeding to proteasomal degradation of Akt, through which mechanism the atherosclerotic plaque instability may be facilitated.