• Journal of the Korean Society of Food Science and Nutrition
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• v.26 no.6
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• pp.1140-1146
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• 1997

Storage stability of ginger paste product was investigated from the standpoint of the inhibition of nonenzymatic browning and loss of gingerol contents. For the experimentations, control, 0.04% of N-acetyl-L-cysteine in ginger paste(NAcCys), and combination treatment of NAcCys, 0.92 of water activity and 6.30 of pH in ginger paste (mixed treatment) were stored at 3$0^{\circ}C$ for 40 days and analyzed for browning and gingerol contents. In addition the changes in sugars, organic acids, ascorbic acids, amino acids, and sensory quality were determined. The results revealed that the mixed treatment agent was effective in preventing both nonenzymatic browning and loss of gingerol contents. The inhibition by combination treatment might be resulted from the control of radical formations by sulfhydryl groups of NAcCys and the increase of diffusion resistance in lower water activity. Browning development and total gingerol contents were found to be correlated to some physicochemical characteristics of ginger paste; that is, browning development to amino acid and color value in sensory evaluation, and total gingerol contents to flavor in sensory evaluation.

• Asian-Australasian Journal of Animal Sciences
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• v.30 no.8
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• pp.1135-1142
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• 2017

Objective: The objective of this study was to evaluate effects of heat treatment and soybean oil inclusion on protein oxidation of soy protein isolate (SPI) and of oxidized protein on redox status of broilers at an early age. Methods: SPI mixed with soybean oil (SPIO) heated at $100^{\circ}C$ for 8 h was used to evaluate protein oxidation of SPI. A total of two hundred and sixteen 1-day-old Arbor Acres chicks were divided into 3 groups with 6 replicates of 12 birds, receiving basal diet (CON), heat-oxidized SPI diet (HSPI) or mixture of SPI and 2% soybean oil diet (HSPIO) for 21 d, respectively. Results: Increased protein carbonyl, decreased protein sulfhydryl of SPI were observed as heating time increased in all treatments (p<0.05). Addition of 2% soybean oil increased protein carbonyl of SPI at 8 h heating (p<0.05). Dietary HSPI and HSPIO decreased the average daily gain of broilers as compared with the CON (p<0.05). Broilers fed HSPI and HSPIO exhibited decreased glutathione (GSH) in serum, catalase activity and total sulfhydryl in liver and increased malondialdehyde (MDA) and protein carbonyl in serum, advanced oxidation protein products (AOPPs) in liver and protein carbonyl in jejunal mucosa as compared with that of the CON (p<0.05). Additionally, broilers receiving HSPIO showed decreased glutathione peroxidase activity (GSH-Px) in serum, GSH and hydroxyl radical scavenging capacity in liver, GSH-Px activity in duodenal mucosa, GSH-Px activity and superoxide anion radical scavenging capacity in jejunal mucosa and increased AOPPs in serum, MDA and protein carbonyl in liver, MDA and AOPPs in jejunal mucosa (p<0.05). Conclusion: Protein oxidation of SPI can be induced by heat and soybean oil and oxidized protein resulted in redox imbalance in broilers at an early age.

• The Korean Journal of Pharmacology
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• v.24 no.2
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• pp.179-187
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• 1988

Verapamil, tetrodotoxin and tetraethylammonium chloride in the stated amount did not affect the $Na^{++}$ induced $Ca^{++}$ release. $Cd^{++}$ and $Zn^{++}$ significantly inhibited the $Na^{++}$ induced $Ca^{++}$ release. $Mn^{++}$ also inhibited $Na^+-Ca^{++}$ exchange. $Cd^{++}$ inhibited $Na^+-Ca^{++}$ exchange noncompetitively with an apparent inhibition constant (Ki) of $100\;{\mu}M$. $Cd^{++}$ caused loss of sulfhydryl group, whereas $Zn^{++}$ did not show any significant effect. $Cd^{++}$ and $Zn^{++}$ effectively inhibited $Na^+-Ca^{++}$ ATPase and slightly inhibited $Ca^{++}-Mg^{++}$ ATPase. Carbonyl cyanide chlorophenylhydrazone, 2,4-dinitrophenol and sodium arsenate stimulated the $Na^{++}$ induced $Ca^{++}$ release. Dibucaine and oligomycin slightly inhibited it. The results suggest that the $Na^+-Ca^{++}$ exchange on the synaptosomal plasma membrane may be not accomplished by ion channels. The $Na^+-Ca^{++}$ exchange is sensitively inhibited by $Cd^{++}$ and this transport process appears to be partially regulated by sulfhydryl groups of the synaptosomal plasma membrane. It is also postulated that $Na^+-Ca^{++}$ exchange is suppressed during the phosphorylation reaction of protein component on the neuronal membrane.

• The Korean Journal of Physiology
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• v.6 no.2
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• pp.57-63
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• 1972

In an attempt to better understand the radioprotective effect of reduced glutathione(GSH), and to observe a possible radioprotective effect of Ginseng extract, whole body X-irradiation of 1,200 r was administered to the mouse either independently or immediately following the injection of GSH or Ginseng extract to the mouse intraperitoneally. The non-protein sulfhydryl (NP-SH) and non-protein disulfide (NP-SS) levels of the liver, and NP-SH level of NP-SH of the blood of the mouse were measured at 30, 60 and 120 minutes, and results were compared with the normal. The results thus obtained are summarized as follows; 1) The normal values of NP-SH and NP-SS of the mouse liver were $5.90{\pm}0.46\;{\mu}\;mol/gm\;wet\;wt.,\;and\;3.02{\pm}0.42\;{\mu}\;mol/ml$ wet wt., respectively, and the normal value of NP-SH of NP-SH of the mouse blood was $3.98{\pm}1.29\;{\mu}\;mol/ml$ 2) The injection of both GSH and Ginseng extract produced the highest values of NP-SH in the liver at 30 minutes, but a gradual decrease to the normal was observed thereafter. When X-irradiation alone was applied, the liver NP-SH value was lower than the normal at 60 minutes post-irradiation and thereafter. When Ginseng extract was injected immediately prior to X-irradiation, the liver NP-SH was lower than the normal throughout the experiment with the lowest value at 60 minutes. However, the combination of GSH and X-irradiation produced higher than the normal values throughout the entire experiment. 3) The liver NP-SS value was most significantly elevated at 30 minutes after the injection of GSH, hut the recovery to the normal was observed thereafter. The injection of Ginseng extract produced slightly higher liver NP-SS values at 30 and 60 minutes, but the value at 120 minutes was similar to the normal. The single application of X-irradiation resulted in the lower then normal liver NP-SS values throughout the entire experiment. When GSH was injected price to X-irradiation, the liver NP-SS values were higher than the normal at 30 and 60 minutes followed b the recovery to the normal at 120 minutes. The combination of Ginseng extract and X-irradiation showed generally lower liver NP-SS values throughout the experiment. 4) The blood NP-SH showed the higher than the normal values in all the experimental groups except when GSH was injected prior to X-irradiation alone produced e significantly elevated blood NP-SS value at 30 minutes post-irradiation.

• The Korean Journal of Pharmacology
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• v.27 no.1
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• pp.69-80
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• 1991

Inhibitory effects of quercetin and rutin on lipid peroxidation of microsomes caused by iron(II) were investigated with respect to the scavenging action for oxygen radicals produced during oxidation of iron and the chelating action for iron. Lipid peroxidation by $Fe^{2+}$ alone was markedly inhibited by quercetin or rutin in a dose dependent fashion. Lipid peroxidation by ascorbate or NADPH in the presence of $Fe^{2+}$ was almost completely inhibited by both quercetin and rutin. The peroxidative action of $Fe^{2+}$ was inhibited by SOD and DABCO and slightly inhibited by catalase, DMSO and mannitol. Quercetin and rutin inhibited oxidation of $Fe^{2+}$ which is responsible for DETAPAC and they showed a significant initial chelating effect. Quercetin and rutin effectively inhibited lipid peroxidation by $H_{2}O_{2}$ and decomposed $H_{2}O_{2}$. Both $OH{\cdot}$ production in the presence of $Fe^{2+}$ and $^1O_2$ production by U.V. irradiation were inhibited by quercetin and rutin. Lipid peroxidations by $Cd^{2+},\;Cu^{2+},\;Ni^{2+},\;Pb^{2+}$ and $Zn^{2+}$ were almost completely inhibited by quercetin. Quercetin and rutin significantly prevented the loss of sulfhydryl groups by $Fe^{2+}$. These results suggest that inhibitory effects of quercetin and rutin on the peroxidative action of $Fe^{2+}$ in the presence or absence of ascorbate and NADPH may be attributable to their scavenging action on reactive oxygen species and chelating action on iron.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.24 no.5
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• pp.443-454
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• 2021

Purpose: Due to the increasing prevalence of obesity worldwide, non-alcoholic fatty liver disease (NAFLD) has reached epidemic dimensions over time. NAFLD is the most common cause of childhood chronic liver disease. There is a relationship between NAFLD and oxidative stress. This study aims to investigate the changes in thiol/disulfide homeostasis parameters to determine the oxidant/antioxidant balance in obese rats with diet-induced NAFLD and healthy rats. Methods: Twelve Wistar albino rats were used in this study. Experimentally produced NAFLD obese rats (n=6) and healthy rats were compared. Experimental NAFLD model was created with a special fatty liver diet (Altromin^® C1063, Fatty Liver Diet, Exclusivet, Lage, Germany). The biochemical and histopathological features of the groups, as well as serum thiol/disulfide homeostasis parameters, were analyzed and compared. Results: In the experimentally induced NAFLD rat model, they gained more weight than the control group. Steatosis (at least grade 2) occurred in all rats fed with special fatty liver diet for 12 weeks. Histopathologically, no high-grade inflammation was observed in rats with experimental NAFLD after feeding a diet for 12 weeks. Results revealed that aspartate transaminase and alanine transaminase levels were high, albumin levels were low, oxidant stress parameters increased, and antioxidant thiol groups decreased. Conclusion: Experimental NAFLD is characterized by increased oxidant stress accompanying fatty tissue in the liver. Analysis of thiol/disulfide homeostasis parameters in NAFLD can be used in further studies to develop effective treatment options.

• Journal of Ginseng Research
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• v.19 no.1
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• pp.31-38
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• 1995

Antioxidant effect of Korean ginseng (Panax ginseng C.A. Meyer) was investigated in rats. Long-term administration of ginseng water extract protected the activity of liver cytosotic SOD, catalase and glutathione peroxidase from being significantly decreased with advancing age (p<0.05). It was more effective toward glutathione peroxidase than other antioxidant enzymes. However, the level of sulfhydryl compounds and its related enzymes such as glutathione reductase and glutathione-5-transferase was not significantly changed by the administration of ginseng. Liver microsomal formation of reactive oxygen species such as superoxide and hydrogen peroxide did not show a significant difference between two groups although it was slightly decreased with age, but lipid peroxidizability of microsomal membrane induced by a prooxidant was slightly lower in ginseng-treated rats. Interestingly, antioxidant capacity of plasma from ginseng treated rats on autooxidation of ok-brain homogenates was much higher than that of normal ones. However, resistance of RBC membrane against oxidative stress showed a similar tendency. The content of serum TBA reactive substances lowered consistently in the rats treated with r ginseng at all corresponding age and a significant difference between two groups was found at 24 months of age (p<0.05). Ginseng extract protected lipid peroxidation in brain and liver. This protection was more effective in the stressed rats imposed by immobilization than normal ones. In conclusion, ginseng water extract protected the age related deterioration of major antioxidant enzymes, and this effect was more striking with increasing duration of treatment. This comprehensive antioxidant action of ginseng seems to be bra certain action of ginseng other than a direct antioxidant action, which might be a long term normalizing effect through the harmony of various components.

• Tuberculosis and Respiratory Diseases
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• v.44 no.1
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• pp.104-113
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• 1997

Background : Toxic oxygen free radicals have been implicated as important pathologic mediators in many clinical disorders. Enhancing the intracellular content of antioxidant enzymes(superoxide dismutase, glutathione peroxidase, and catalase) can provide means of limiting biological damage caused by oxygen free radicals. The oxygen free radicals and changes of antioxidant enzymes are though to play a role in the pathogenesis of chronic obstructive pulmonary disease. Method : To investigate the pulmonary oxygen radical injury and the protective role of antioxidant enzymes in Chronic obstructive pulmonary disease(COPD), author measured the amount of thiobarbituric acid reactants, the activities of antioxidant enzymes and the sulfhydry1 groups of glutathione in serum and red blood cells from the patients with COPD(COPD patients) and the normal controls. Results : The thiobarbituric acid reactant in serum and red blood cells of COPD patients was increased than those of the normal controls, and the superoxide dismutase activity in red blood cells was no statistical difference in both groups. But the glutathione peroxidase and catalase activities in red blood cel1s of COPD patients were significantly lowered than those of the normal controls. The sulfhydry1 groups in serum and red blood cells were no statistically difference in both groups. Conclusion : These results suggest that the increased thiobarbituric acid reactants in serum and RBCs of chronic obstructive pulmonary disease mean oxygen radical toxicity, and the decreased glutathione peroxidase and catalase activities in RBC could take pan in pathogenesis of chronic obstructive pulmonary disease.

• Journal of Nutrition and Health
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• v.31 no.2
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• pp.213-219
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• 1998

This study was conducted to compare and evaluate the iodide specific ion electrode method (ISE) and neutron activation analysis method (NAA) for determining iodine in human milk and cow milk. The neutron irradiation and counting operations were carried out at the TRIGA Mark-III reactor facility of the Korea Atomic Energy Research Institute. The mean concentrations of iodine in human milk samples by the ISE and the NAA were 1450$\mu\textrm{g}$/L and 1350$\mu\textrm{g}$/L, respectively. The levels were not significantly different. In cow milk samples , the mean concentrations of iodine by the ISE and the NAA were 250$\mu\textrm{g}$.L and 200$\mu\textrm{g}$/L, respectively. here, the ISE reading was significantly higher than the NAA. reading. The correlations of the two methods were 0.92(p<0.001) for human milk samples and 0.65 for cow milk samples . The coefficient of variation was 8.3% in the ISE and 4.9% in the NAA. Therefore, the iodide specific ion electrode method is sample and fast method, but probably not in processed milk since free sulfhydryl groups in milk are also detected by the iodide electrode. However, these also indicate that the ISE method may be applicable to human milk and pasteurized milk if the conventional pasteurization time-temperature relationship of standards is not exceeded. On the other hand, the NAA method , which is independent of chemical forms and matrix, can be used for determining iodine in all kinds of milk and foods.

• BMB Reports
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• v.45 no.11
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• pp.671-676
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• 2012

Caloric restriction (CR) has been associated with health benefits and these effects have been attributed, in part, to modulation of oxidative status by CR; however, data are still controversial. Here, we investigate the effects of seventeen weeks of chronic CR on parameters of oxidative damage/modification of proteins and on antioxidant enzyme activities in cardiac and kidney tissues. Our results demonstrate that CR induced an increase in protein carbonylation in the heart without changing the content of sulfhydryl groups or the activities of superoxide dismutase and catalase (CAT). Moreover, CR caused an increase in CAT activity in kidney, without changing other parameters. Protein carbonylation has been associated with oxidative damage and functional impairment; however, we cannot exclude the possibility that, under our conditions, this alteration indicates a different functional meaning in the heart tissue. In addition, we reinforce the idea that CR can increase CAT activity in the kidney. Moreover, CR caused an increase in CAT activity in kidney, without changing other parameters. Protein carbonylation has been associated with oxidative damage and functional impairment; however, we cannot exclude the possibility that, under our conditions, this alteration indicates a different functional meaning in the heart tissue. In addition, we reinforce the idea that CR can increase CAT activity in the kidney.