• Journal of the Korean Society of Propulsion Engineers
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• v.16 no.1
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• pp.1-8
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• 2012

Acoustic-pressure response of diluted hydrogen-air diffusion flames is investigated numerically by adopting a fully unsteady analysis of flame structures in low and high pressure regimes. As acoustic frequency increases, finite-rate chemistry is enhanced through a nonlinear accumulation of heat release rate for any pressure regime, leading to a high amplification index. Same numerical results are analyzed with application of a pressure-sensitive time lag model, and thereby, interaction index and time lag are calculated for each pressure regime. The interaction index has the largest value in each pressure regime at an acoustic frequency near 1000 Hz. In a high-pressure regime, flames are more unstable than in a low-pressure regime. The interaction index shows a good agreement with the amplification index.

• Biomedical Science Letters
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• v.6 no.1
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• pp.45-53
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• 2000

The anti-oxidative effects of Korean red ginseng extracts (total saponine, water extracts, alcohol extracts, lipophilic extracts), which were administered with the concentration of 200 mg/kg BW, were investigated after the injection of paraquat (1,1-dimethyl-4,4-bipyrimidinium dichloride: PQ) with dosage of 100 mg/kg BW on the peritoneal cavity to 6 weeks of 23~26 gm ICR male mice. The accumulation of hydrogen peroxide ($H_2O$$_2$) on the liver of mouse was lowered only in alcohol extract-treated group (p<0.05). The activity of glutathione peroxidase increased in the mouse treated with lipophilic ginseng extracts. And GSSG level was lowered in all groups, and this might be due to the paraquat ions that might prevent the reaction of GSSG into GSH. But we cannot find any relation between glutathione oxide-reductase activity on Korean ginseng extracts. Finally, the lipid peroxidation (MDA) level was lowest (p<0.01) in the group of mouse treated with water extracts of ginseng.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.1
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• pp.51-58
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• 2006

The promoting effect of hydrogen peroxide ($H_2O_2$) against the cytotoxicity of 1-methyl-4-phenylpyridinium ($MPP^+$) in differentiated PC12 cells was assessed by measuring the effect on the mitochondrial membrane permeability. Treatment of PC12 cells with $MPP^+$ resulted in the nuclear damage, decrease in the mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c, activation of caspase-3, increase in the formation of reactive oxygen species (ROS) and depletion of GSH. Addition of $H_2O_2$ enhanced the $MPP^+-induced$ nuclear damage and cell death. Catalase, Carboxy-PTIO, Mn-TBAP, N-acetylcysteine, cyclosporin A and trifluoperazine inhibited the cytotoxic effect of $MPP^+$ in the presence of $H_2O_2$. Addition of $H_2O_2$ promoted the change in the mitochondrial membrane permeability, ROS formation and decrease in GSH contents due to $MPP^+$ in PC12 cells. The results show that the $H_2O_2$ treatment promotes the cytotoxicity of $MPP^+$ against PC12 cells. $H_2O_2$ may enhance the $MPP^+$-induced viability loss in PC12 cells by promoting the mitochondrial membrane permeability change, release of cytochrome c and subsequent activation of caspase-3, which is associated with the increased formation of ROS and depletion of GSH. The findings suggest that $H_2O_2$ as a promoting agent for the formation of mitochondrial permeability transition may enhance the neuronal cell injury caused by neurotoxins.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.2
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• pp.85-94
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• 2006

A splanchic artery occlusion for 90 min followed by reperfusion of the mesenteric circulation resulted in a severe form of circulatory shock, characterized by endothelial dysfunction, severe hypotension, marked intestinal tissue injury, and a high mortality rate. The effect of defibrotide, a complex of single-stranded polydeoxyribonucleotides having antithrombotic effect, was investigated in a model of splanchnic artery occlusion (SAO) shock in urethane anesthetized rats. Occlusion of the superior mesenteric artery for 90 min produced a severe shock state, resulting in a fatal outcome within 120 min of reperfusion in many rats. Defibrotide (10 mg/kg body weight) 10 min prior to reperfusion significantly improved mean arterial blood pressure in comparison to vehicle treated rats (p＜0.05). Defibrotide treatment also significantly attenuated in the increase of plasma amino nitrogen concentration, intestinal myeloperoxidase activity, intestinal lipid peroxidation, infiltration of neutrophils in intestine and thrombin induced adherence of neutrophils to superior mesentric artery segments. Superoxide anion and hydrogen peroxide production in $1{\mu}M$ formylmethionylleucylphenylalanine (fMLP)-activated PMNs was inhibited by defibrotide in a dose-dependent fashion. Defibrotide effectively scavenged hydrogen peroxide, but not hydroxyl radical. Treatment of SAO rats with defibrotide inhibited tumor necrosis factor-${\alpha}$, and interleukin-1${\beta}$ productions in blood in comparison with untreated rats. These results suggest that defibrotide partly provides beneficial effects by preserving endothelial function, attenuating neutrophil accumulation, and antioxidant in the ischemic reperfused splanchnic circulation

• Korean Journal of Pharmacognosy
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• v.46 no.2
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• pp.116-122
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• 2015

Keratinocytes are first barrier against outer challenges on skin. However, it is still largely unknown about effective protectors against ultraviolet B (UVB), and oxidative stress in human keratinocyte, HaCaT cells. Inducible heme oxygenase (HO)-1 acts against oxidants that are thought to play a role in the pathogenesis of skin disorders. Therefore, the purpose of this study was to evaluate the effect of Portulaca oleracea 70% EtOH extracts against hydrogen peroxide (H₂O₂)-induced oxidative stress in human keratinocytes, HaCaT cells. P. oleracea 70% EtOH extracts showed the potent protective effects on H₂O₂-induced toxicity by induced the expression of HO-1 in human keratinocyte, HaCaT cells. Furthermore, P. oleracea 70 % EtOH extracts caused the nuclear accumulation of nuclear factor E2-related factor 2 (Nrf2) in human keratinocytes, HaCaT cells. In addition, we found that treatment with c-Jun N-terminal kinase (JNK) inhibitor (SP600125) reduced P. oleracea 70% EtOH extracts-induced HO-1 expression, and JNK inhibitor (SP600125) also inhibited protective effects by P. oleracea 70% EtOH extracts. Therefore, these results suggest that P. oleracea 70 % EtOH extracts increases cellular resistance to H₂O₂-induced oxidative injury in human keratinocyte, HaCaT cells, presumably through JNK pathway-Nrf2-dependent HO-1 expression.

• Journal of Microbiology and Biotechnology
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• v.28 no.12
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• pp.1982-1991
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• 2018

Ethanol accumulation inhibited the growth of Saccharomyces cerevisiae during wine fermentation. Autophagy and the release of reactive oxygen species (ROS) were also induced under ethanol stress. However, the relation between autophagy and ethanol stress was still unclear. In this study, expression of the autophagy genes ATG1 and ATG8 and the production of ROS under ethanol treatment in yeast were measured. The results showed that ethanol stress very significantly induced expression of the ATG1 and ATG8 genes and the production of hydrogen peroxide ($H_2O_2$) and superoxide anion (${O_2}^{{\cdot}_-}$). Moreover, the atg1 and atg8 mutants aggregated more $H_2O_2$ and ${O_2}^{{\cdot}_-}$ than the wild-type yeast. In addition, inhibitors of the ROS scavenging enzyme induced expression of the ATG1 and ATG8 genes by increasing the levels of $H_2O_2$ and ${O_2}^{{\cdot}_-}$. In contrast, glutathione (GSH) and N-acetylcystine (NAC) decreased ATG1 and ATG8 expression by reducing $H_2O_2$ and ${O_2}^{{\cdot}_-}$ production. Rapamycin and 3-methyladenine also caused an obvious change in autophagy levels and simultaneously altered the release of $H_2O_2$ and ${O_2}^{{\cdot}_-}$. Finally, inhibitors of the mitochondrial electron transport chain (mtETC) increased the production of $H_2O_2$ and ${O_2}^{{\cdot}_-}$ and also promoted expression levels of the ATG1 and ATG8 genes. In conclusion, ethanol stress induced autophagy which was regulated by $H_2O_2$ and ${O_2}^{{\cdot}_-}$ derived from mtETC, and in turn, the autophagy contributed to the elimination $H_2O_2$ and ${O_2}^{{\cdot}_-}$.

• Journal of the Korea Organic Resources Recycling Association
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• v.11 no.4
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• pp.105-113
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• 2003

Successful operation of a reactor can be accomplished when it is operated at proper D depending on the state of degradation. Operation at high D leads to the washout of biomass in the reactor while operation at low D leads to product inhibition due to the accumulation of excess VFA. These appear to limit the production of hydrogen to reach a higher level. Operation by D control was performed to improve the efficiency of hydrogen fermentation of food waste. Although simple organic matters were rapidly degraded in the early stage (day 1-2), proper VFA concentration and pH values were kept in the reactor at D of $4.5d^{-1}$, which was previously reported to be optimum initial D. High butyrate/acetate (B/A) ratios over 3.2 were obtained. Without D control, the reduction of simple organic matters after day 2 caused the decrease of VFA production and the increase of pH. Hydrogen production also decreased, as microbial proliferation was less than microbial loss by washout. However, the reactor performance was dramatically improved at D control from 4.5 to $2.3d^{-1}$. It showed the highest B/A ratios over 2.0 among the reactors on day 4-7. The second hydrogen peak appeared on day 4, resulting in the highest fermentation efficiency (70.8%) among the reactors. It was caused by the enhanced degradation of slowly degradable matters. The COD removed was converted to hydrogen (19.3%), VFA (36.5%), and ethanol (15.0%). Therefore, the strategy using D control, depending on the state of degradation, was effective in improving the efficiency of hydrogen fermentation.

• Journal of Dairy Science and Biotechnology
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• v.38 no.3
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• pp.134-141
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• 2020

Oxidative stress is a cascade reaction characterized by a significant increase in the amount of oxidized components. Free radicals produced by oxidative stress are one of the common features in several experimental models of disease, and contribute to wide range of neurodegenerative diseases, including Alzheimer's disease. Iron (II) species can participate in the Fenton, and Fenton-like reactions, to react with hydrogen peroxide and generate hydroxyl radical. As iron accumulation and oxidative stress are associated with the pathological progression of neurodegenerative diseases, iron chelation and antioxidant therapies have become strategies to combat these diseases. Due to the complexity of the redox system in vivo, a multifaceted approach may be an attractive therapeutic strategy. Further investigations are highly expected for the prevention and treatment of neurodegenerative diseases in future.

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2003.10a
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• pp.100.2-101
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• 2003

The global regulator, GacS (global antibiotic and cyanide sensor kinase), was required for the increased resistance to hydrogen peroxide occurring as cultures of the rhizobacterium, P. chlororaphis O6, matured. Specific stationary-phase peroxidase and catalase isozymes were absent in the GacS mutant, whereas a manganese-superoxide dismutase isozyme was expressed earlier and to a great extent than wild type. In the wild type cell, transcript accumulation of rpoS was higher in late logarithmic-phase cells than cells from mid logarithmic- or stationary-phase. Transcripts from rpoS in the GacS mutant were reduced in each of these growth phases compared to the wild type expression. The down stream sequence from rpoS lacked sequences encoding a small RNA, rsmZ, found in other pseudomonads and implicated in control of genes activated by the GacS system. These findings suggest that GacS-mediated regulation of RpoS plays role in control of oxidative stress in P. chlororaphis O6 by as yet an unknown mechanism.

• Journal of Acupuncture Research
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• v.15 no.2
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• pp.135-145
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• 1998

Bupleury radix has been used for the treatment of fever, liver disease, inflammation in traditional medicine. The present study was carried out to evaluate the antioxidant effects of Bupleury radix aqua-acupuncture solution (BRAS) in vitro. Oxygen derived free radicals produced in the course of normal aerobic life, such as superoxide anion radical($O_2^-$ ), hydroxyl radicaI( OH), hydrogen peroxide($H_2O_2$) and singlet oxygen($^1O_2$) can attack polyunsaturated fatty acid in cell membranes, enzymes, other cell compounds, and give rise to lipid peroxidation, DNA damage, lipofuscin accumulation, structure alteration of cell membrane and cell death. In this study, antioxidant effects of BRAS on lipid peroxidation were determined according to the method of TBA. BRAS inhibited markedly peroxidation of linoleic acid during the autoxidation, and also inhibited lipid peroxidation induced by hydroxyl radical derived from $H_2O_2-Fe^{2+}$ in rat liver homogenate. And BRAS showed 30% scavenging effect on DPPH radical, also exhibited a 30% inhibitory effect on superoxide generation from xanthine-xanthine oxidase system. In addition, BRAS protected the cell death induced by tert-butyl hydroperoxide(t-BHP) and significantly increased cell viability in the normal rat liver cell(Ac2F).