• 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 the Korean Society of Food Science and Nutrition
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• v.42 no.10
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• pp.1525-1532
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• 2013

The objective of this study was to investigate the effect of hot water extract from Cornus walteri Wanger (CWE) on tert-butyl hydroperoxide (TBHP)-induced oxidative stress in HepG2 cells. Generation of reactive oxygen species (ROS), concentrations of cellular lipid peroxidation products and reduced glutathione, and antioxidant enzyme activity were used as biomakers of cellular oxidative status. Cells pretreated with CWE (25~200 ${\mu}g/mL$) showed an increased resistance to oxidative stress in a dose-dependent manner, as revealed by a higher percentage of surviving cells compared to control cells. ROS generation induced by TBHP was significantly reduced when cells were pretreated with 200 ${\mu}g/mL$ CWE for 4 h. Pretreatment with CWE (5~50 ${\mu}g/mL$) prevented the decrease in reduced glutathione and the increase in malondialdehyde and ROS evoked by TBHP in HepG2 cells. Finally, CWE pretreatments prevented the significant increase of glutathione peroxidase, catalase, glutathione reductase, and superoxide dismutase activities induced by TBHP. These results show that CWE has significant protective ability against a TBHP-induced oxidative insult and that the modulation of antioxidant enzymes by CWE may have an important antioxidant effect on TBHP-induced oxidative stress in HepG2 cells.

• Journal of Ecology and Environment
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• v.30 no.4
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• pp.307-314
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• 2007

We studied changes in the biochemical and physiological status and ROS-scavenging enzyme (superoxide dismutase, catalase and peroxidase) activity in leaves and roots of rice (Oryza sativa L.) plants exposed to high salinity. Under salt stress, the reduction in RWC (relative water content) in leaves was relatively severe in comparison with that of roots. The proline content was also significantly higher in leaves of rice plants following salt treatment. The activities of CAT and POX in roots increased with increasing NaCl concentration, but the activity of SOD decreased. These results suggest that the increase of endogenous proline is closely associated with the increase of CAT and POX activities, which may play important roles in salt tolerance. Therefore, we conclude that the alleviation of oxidative damage and increased resistance to salinity may result from the presence of efficient antioxidative systems.

• BMB Reports
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• v.36 no.3
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• pp.282-287
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• 2003

The production of superoxide dismutase (SOD) varied in Deinococcus radiophilus, the UV resistant bacterium, depending upon different phases of growth, UV irradiation, and superoxide treatment. A gradual increase in total SOD activity occurred up to the stationary phases. The electrophoretic resolution of the SOD in cell extracts of D. radiophilus at each growth phase revealed the occurrence of MnSOD throughout the growth phases. The SOD profiles of D. radiophilus at the exponential phase received oxidative stress by the potassium superoxide treatment or UV irradiation also revealed the occurrence of a single SOD. However, these treatments caused an increase in SOD activity. The data strongly suggest that D. radiophilus has only one species of SOD as a constitutive enzyme, which seems to be a membrane-associated protein.

• Archives of Pharmacal Research
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• v.21 no.1
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• pp.46-53
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• 1998

When NIH3T3 cells were exposed to mild heat and recovered at $37^{\circ}C$ for various time intervals, they were thermotolerant and resistant to subsequent stresses including heat, oxidative stresses, and antitumor drug methotrexate which are apoptotic inducers. The induction kinetics of apoptosis by stresses were determined by DNA fragmentation and protein synthesis using $[35^S]$methionine pulse labeling. We investigated the hypothesis that thermotolerant cells were resistant to apoptotic cell death compared to control cells when both cells were exposed to various stresses inducing apoptosis. The cellular changes in thermotolerant cells were examined to determine which components are involved in this resistance. At first, the degree of resistance correlates with the extent of heat shock protein synthesis which were varied depending on the heating times at $45^{\circ}C$ and recovery times at $37^{\circ}C$after heat shock. Secondly, membrane permeability change was observed in thermotolerant cells. When cells prelabeled with $[^{3}H]$thymidine were exposed to various amounts of heat and recovered at $37^{\circ}C$ for 1/2 to 24 h, the permeability of cytosolic $[^{3}H]$thymidine in thermotolerant cells was 4 fold higher than that in control cells. Thirdly, the protein synthesis rates in thermotolerant and control cells were measured after exposing the cells to the same extent of stress. It turned out that thermotolerant cells were less damaged to same amount of stress than control cells, although the recovery rates are very similar to each other. These results demonstrate that an increase of heat shock proteins and membrane changes in thermotolerant cells may protect the cells from the stresses and increase the resistance to apoptotic cell death, even though the exact mechanism should be further studied.

• BMB Reports
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• v.42 no.8
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• pp.475-481
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• 2009

Emerging data demonstrate pivotal roles for brain insulin resistance and insulin deficiency as mediators of cognitive impairment and neurodegeneration, particularly Alzheimer's disease (AD). Insulin and insulin-like growth factors (IGFs) regulate neuronal survival, energy metabolism, and plasticity, which are required for learning and memory. Hence, endogenous brain-specific impairments in insulin and IGF signaling account for the majority of AD-associated abnormalities. However, a second major mechanism of cognitive impairment has been linked to obesity and Type 2 diabetes (T2DM). Human and experimental animal studies revealed that neurodegeneration associated with peripheral insulin resistance is likely effectuated via a liver-brain axis whereby toxic lipids, including ceramides, cross the blood brain barrier and cause brain insulin resistance, oxidative stress, neuro-inflammation, and cell death. In essence, there are dual mechanisms of brain insulin resistance leading to AD-type neurodegeneration: one mediated by endogenous, CNS factors; and the other, peripheral insulin resistance with excess cytotoxic ceramide production.

• Integrative Medicine Research
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• v.2 no.4
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• pp.131-138
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• 2013

The skeletal muscle in our body is a major site for bioenergetics and metabolism during exercise. Carbohydrates and fats are the primary nutrients that provide the necessary energy required to maintain cellular activities during exercise. The metabolic responses to exercise in glucose and lipid regulation depend on the intensity and duration of exercise. Because of the increasing prevalence of obesity, recent studies have focused on the cellular and molecular mechanisms of obesity-induced insulin resistance in skeletal muscle. Accumulation of intramyocellular lipid may lead to insulin resistance in skeletal muscle. In addition, lipid intermediates (e.g., fatty acyl-coenzyme A, diacylglycerol, and ceramide) impair insulin signaling in skeletal muscle. Recently, emerging evidence linking obesity-induced insulin resistance to excessive lipid oxidation, mitochondrial overload, and mitochondrial oxidative stress have been provided with mitochondrial function. This review will provide a brief comprehensive summary on exercise and skeletal muscle metabolism, and discuss the potential mechanisms of obesity-induced insulin resistance in skeletal muscle.

• Korean journal of food and cookery science
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• v.30 no.4
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• pp.369-377
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• 2014

Obesity increases oxidative stress, which could contribute to the development of insulin resistance and hyperglycemia. The purpose of this study was to investigate the hypoglycemic and antioxidant effect of sanchae-namul (SN) in mice with diet-induced obesity. Five-week-old male C57BL/6J mice were fed a basal or high-fat and high-sucrose (HFHS) diet with or without 3% freeze-dried SN powder composed of chamnamul, daraesoon, miyeokchwi, bangpung namul, and samnamul for 12 weeks after a 1-week adaptation. After sacrifice, serum glucose and insulin were measured and the homeostasis model assessment for insulin resistance (HOMA-IR) was determined as well. Hepatic lipid peroxidation, glutathione (GSH), and activities of the antioxidant enzymes were determined. SN given at 3% of the total diet did not significantly influence body weight and food intake in mice fed the HFHS diet. Serum glucose and insulin levels, as well as HOMA-IR values, were significantly lower in the SN group than those in the HFHS group. Thiobarbituric acid reactive substances (TBARS) levels in the liver were decreased significantly in the SN group compared with those in the HFHS group. SN significantly increased the GSH levels and the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in the liver compared with those in the HFHS group. Overall, these findings suggest that SN may be useful in alleviating insulin resistance and hyperglycemia in mice fed HFHS diet; further, the improvement of insulin resistance could partly occur by reducing the oxidative stress.

• Asian-Australasian Journal of Animal Sciences
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• v.23 no.5
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• pp.588-597
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• 2010

We investigated the effect of quercetin on growth and plasma cholesterol level and the effects of quercetin pretreatment (Diet 1, 0%; Diet 2, 0.25%; and Diet 3, 0.5% quercetin) for 30 and 60 days on oxidative stress induced by hypo-osmotic conditions (17.5, 8.75, and 4 psu) in olive flounder. The weights of flounder were higher with Diet 3 than with Diet 1 and 2, which indicated that a high concentration (Diet 3) of quercetin was very effective in growth. Total cholesterol levels were lower with Diets 2 and 3 than with Diet 1, leading us to hypothesize that quercetin removed low-density lipoproteins from circulation and thereby reduced total cholesterol. To understand the antioxidant role of quercetin, we measured the mRNA expression and activities of superoxide dismutase (SOD) and catalase (CAT) and the $H_2O_2$ concentration in quercetin-treated flounder exposed to osmotic stress. The $H_2O_2$ concentration and the SOD and CAT expression and activity levels were lower in flounder fed with Diets 2 and 3 than with Diet 1, suggesting that quercetin directly scavenges reactive oxygen species to reduce oxidative stress. Furthermore, the plasma lysozyme activity and osmolality were higher with Diets 2 and 3 than with Diet 1, indicating that quercetin increases immune function and helps to maintain physiological homeostasis. Plasma cortisol was lower with Diets 2 and 3 than with Diet 1, suggesting the quercetin protects against stress. These results indicate that quercetin has hypocholesterolemic and antioxidant effects, increases immune function, and acts to maintain physiological homeostasis.

• FLOWER RESEARCH JOURNAL
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• v.19 no.4
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• pp.269-273
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• 2011

This study was conducted to investigate the resistance to abiotic stress in the progeny obtained by a cross between NDPK2-transgenic line (NDPK2-7-1) and MnSOD (SOD2) transgenic line (SOD2-2-1-1-35) to develop transgenic petunia highly resistant to environmental stress. At the treatment of 100 and $200{\mu}M$ methyl viologene (MV), the progeny was significantly less damaged than its parental plants (SOD2- or NDPK2-transgenic lines) as well as non-transgenic plants, implying its resistance to oxidative stress enhanced than SOD2- or NDPK2-transgenic plants. In an expression of 11 quantitative traits, the progeny remained similar to control plants, although it infrequently displayed slightly longer or wider than non-transgenic control plants. In the color and shape of flowers, there was no significant difference between the progeny and its parents or non-transgenic control.