• Journal of Environmental Science International
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• v.16 no.12
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• pp.1345-1353
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• 2007

The effect of salicylic acid(SA) on antioxidant system and protective mechanisms against UV-B induced oxidative stress was investigated in cucumber(Cucumis sativus L.) leaves. UV-B radiation and SA were applied separately or in combination to first leaves of cucumber seedlings, and dry matter accumulation, lipid peroxidation and activities of antioxidant enzymes were measured in both dose and time-dependant manner. UV-B exposure showed reduced levels of fresh weight and dry matter production, whereas SA treatment significantly increased them. SA noticeably recovered the UV-B induced inhibition of biomass production. UV-B stress also affected lipid peroxidation and antioxidant enzyme defense system. Malondialdehyde(MDA), a product of lipid peroxidation, was greatly increased under UV-B stress, showing a significant enhancement of a secondary metabolites, which may have antioxidative properties in cucumber leaves exposed to UV-B radiation. Combined application of UV-B and SA caused a moderate increase in lipid peroxidation. These results suggest that SA may mediate protection against oxidative stress. UV-B exposure significantly increased SOD, APX, and GR activity compared with untreated control plants. Those plants treated with 1.0 mM SA showed a similar pattern of changes in activities of antioxidant enzymes. SA-mediated induction of antioxidant enzyme activity may involve a protective accumulation of $H_2O_2$ against UV-B stress. Moreover, their activities were stimulated with a greater increase by UV-B+SA treatment. The UV-B+SA plants always presented higher values than UV-B and SA plants, considering the adverse effects of UV-B on the antioxidant cell system. ABA and JA, second messengers in signaling in response to stresses, showed similar mode of action in UV-B stress, supporting that they may be important in acquired stress tolerance. Based on these results, it can be suggested that SA may participates in the induction of protective mechanisms involved in tolerance to UV-B induced oxidative stress.

• Journal of the Korean Society of Tobacco Science
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• v.31 no.1
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• pp.29-38
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• 2009

Although prion diseases, a group of fatal neurodegenerative diseases of human and animals, are presumed to be caused by several mechanisms including abnormal change of prion protein, oxidative stress is still believed to play a central role in development of the diseases. Cigarette smoking has a few beneficial effects on neuronal diseases such as Alzheimer's disease and Parkinson's disease despite of many detrimental effects. In this study, we investigated how chronic cigarette smoking could exert such beneficial effect against oxidative damage. For this study, homogenates of 87V scrapie-infected brain was inoculated on intracerebral system of IM mice through stereotaxic microinjection and biochemical properties concerning with oxidative stress were examined. The scrapie infection decreased the activity of mitochondrial Mn-containing superoxide dismutase by 50% of the control, meanwhile the effects on other antioxidant enzymes including Cu or Zn-containing superoxide dismutase were not significant. Additionally, the infection elevated superoxide level as well as monoamine oxide-B (MAO-B) in the infected brain. Interestingly, many of the detrimental effects were improved in partial or significantly by long-term cigarette smoke exposure (CSE). CSE not only completely prevented the generation of mitochondrial superoxide but also significantly (p<0.05) decreased the elevated mitochondrial MAO-B activity in the infected brain. Concomitantly, CSE prevented subsequent protein oxidation and lipid peroxidation caused by scrapie infection; however, it did not affect the activities of antioxidant enzymes. These results suggest that chronic exposure of cigarette smoke contribute to in part preventing the progress of neurodegeneration caused by scrapie infection.

• Journal of Radiation Industry
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• v.5 no.2
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• pp.125-130
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• 2011

The purpose of this study was to evaluate the protective effect of the Perilla frutescens cv. Chookyoupjaso mutant water extract (PFWE) on gamma ray-induced oxidative stress in mice. Gamma-ray is one of the sources for inducing oxidative stress. The study was divided into 6 groups with 6 mice for each treatment. Groups I and II were treated with saline (vehicle) only, groups III, IV, V, and VI were pretreated with PFWE 10, 20, 50, $50mg\;kg^{-1}$ respectively for 2 weeks before gamma radiation. And then groups II, III, IV, V were irradiated. We found that the activities of aspartate transaminase (AST) and alanine transaminase (ALT) were increased and the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) were decreased by irradiation in mice. However, treatment of PFWE attenuated the activities of AST and ALT in a dose-dependent manner in irradiated mice. Furthermore, treatment of PFWE significantly increased the activities of SOD, GPx, and GR in a dose-dependent manner in irradiated mice, except for the CAT. Interestingly, the activities of GPx and GR were significantly increased by PFWE treatment. Taken together, PFWE could be effective in protecting on gamma ray-induced oxidative stress in mice.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.47 no.6
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• pp.874-881
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• 2014

A laboratory experiment was conducted to determine chronic effects of waterborne copper exposure on rock bream Oplegnathus fasciatus using a panel of enzymes. The activities of the following biochemical biomarkers were determined at different concentrations of $CuSO_4$ for 10 and 20 days: alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) in plasma; antioxidant enzymes including glutathione (GSH), superoxide dismutase (SOD) and glutathione peroxidase (GPx) in liver and gills; and acethylcholinesterase (AChE) in brain and muscle. After exposure to two $CuSO_4$ concentrations (200 and $400{\mu}g/L$), the activities of plasma ALT in the fish showed a tendency to increase with AST and LDH, depending on $CuSO_4$ concentration. Additionally, GSH levels and SOD activities significantly increased, depending on $CuSO_4$ concentrations in liver and gills. This involved the inactivation of reactive molecules formed during oxidative stress, which could provide protection against oxidative damage induced by $CuSO_4$. However, GPx and AChE activities significantly decreased with $CuSO_4$ in liver and gills. In conclusion, these enzymes may represent convenient biomarkers for monitoring heavy metal pollution in coastal areas. Such chronic exposure studies are necessary for improving our understanding of complementary or deleterious effects of pollutants, and for developing metal toxicity biomarkers.

• 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.

• Natural Product Sciences
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• v.29 no.2
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• pp.67-73
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• 2023

Oxidative stress brings about apoptosis through various mechanisms. In particular, oxidative stress in neuronal cells can causes a variety of brain diseases. This study was conducted to investigate the effect of Bidens tripartita on oxidative stress in neuronal cells. B. tripartita has traditionally been used in Russia as a medicine for diseases such as rhinitis, angina and colitis. Over-production of glutamate induces oxidative stress. When the oxidative stress occurs in the cells, reactive oxygen species (ROS) and Ca²⁺ increase. In addition, the abrupt decline of mitochondrial membrane potential and the decrease of glutathione related enzymes such as glutathione reductase (GR) and glutathione peroxidase (GPx) are also observed. The samples used in the experiment showed cytoprotective effect in the MTT assay. It also lowered the ROS and Ca²⁺ level, and increased degree of mitochondrial membrane potential, GR and GPx. As a result, B. tripartita had a positive effect against oxidative stress. Thus, it is expected to have potential for treatment and prevention of degenerative brain diseases such as Alzheimer's disease.

• Proceedings of the KSCN Conference
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• 2003.05a
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• pp.143-143
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• 2003

Reactive oxygen species are highly reactive oxidant molecules and react with cellular components, causing oxidative damages. These damages may play a significant role in the causation of several chronic diseases. Antioxidative defence systems are present in the body to protect cells from oxidative damages. The first line of defence include dietary antioxidants and enzymes such as superoxide dismutase. Cynanchum wilfordii Hemeseley has been used for centuries as a tonic nutraceutical in China and Korea. (omitted)

• Journal of Plant Biology
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• v.12 no.2
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• pp.15-22
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• 1969

By spectrophotometric assay method, the following enzymes could be detected in Dunaliella tertiolecta and Chlorella pyrenoidosa cell-free extracts: Hexokinase; Glucose-6-phosphate, 6-Phosphogluconate and Triosephosphate dehydrogenase; Transketolase; Phosphogluco and Ribosephosphate isomerase; Phosphoglucomutase; Phosphofructokinase; Fructosediphosphate aldorase and Ribulosephosphate 3-epimerase. Such enzymes are in accordance with the proposed pathway of glucose catabolism by D. tertiolecta as well as C. pyrenoidosa. Also, it could be estimated, under the presence of NADP, that pentose phosphate pathway were more active than glycolytic pathway in D. tertiolecta cell-free systems.

• Proceedings of the Korean Biophysical Society Conference
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• 1997.07a
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• pp.15-15
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• 1997

Recent studies indicate that hydrogen peroxide (H$_2$O$_2$), which is one of the reactive oxygen species involved in the oxidative stress, is an intracellular secondary messenger in the signal transduction. A novel family of thiol specific antioxidant (TSA) enzymes with a peroxidase activity shows no sequence homology to previously known antioxidant enzymes.(omitted)

• Journal of Microbiology
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• v.41 no.3
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• pp.248-251
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• 2003

Glutathione (GSH) is an important factor in determining tolerance against oxidative stress in living organisms. It is synthesized in two sequential reactions catalyzed by ${\gamma}$-glutamylcysteine synthetase (GCS) and glutathione synthetase (GS) in the presence of ATP. In this work, the effects of three different oxidative stresses were examined on GSH content and GSH-related enzyme activities in the fission yeast Schizosaccharomyces pombe. GSH content in S. pombe was significantly enhanced by treatment with hydrogen peroxide, ${\beta}$-naphthoflavone (BNF) and tert-butylhydroquinone (BHQ). Simultaneously, they greatly induced GCS and GS activity. However, they did not have any effects on glutathione reductase activity. These results suggest that GCS and GS activities in S. pombe are up-regulated by oxidative stress.