• Archives of Pharmacal Research
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• v.29 no.7
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• pp.577-581
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• 2006

Oxidative mechanisms are thought to have a major role in cataract formation and diabetic complications. Antioxidant enzymes play an essential role in the antioxidant system of the cells that work to maintain low steady-state concentrations of the reactive oxygen species. When HLE-B3 cells, a human lens cell line were exposed to 50-100 mM glucose for 3 days, decrease of viability, inactivation of antioxidant enzymes, and modulation of cellular redox status were observed. Significant increase of cellular oxidative damage reflected by lipid peroxidation and DNA damage were also found. The glycation-mediated inactivation of antioxidant enzymes may result in the perturbation of cellular antioxidant defense mechanisms and subsequently lead to a pro-oxidant condition and may contribute to various pathologies associated with the long term complications of diabetes.

• Biomolecules & Therapeutics
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• v.21 no.2
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• pp.89-96
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• 2013

Atherosclerotic vascular dysfunction is a chronic inflammatory process that spreads from the fatty streak and foam cells through lesion progression. Therefore, its early diagnosis and prevention is unfeasible. Reactive oxygen species (ROS) play important roles in the pathogenesis of atherosclerotic vascular disease. Intracellular redox status is tightly regulated by oxidant and antioxidant systems. Imbalance in these systems causes oxidative or reductive stress which triggers cellular damage or aberrant signaling, and leads to dysregulation. Paradoxically, large clinical trials have shown that non-specific ROS scavenging by antioxidant vitamins is ineffective or sometimes harmful. ROS production can be locally regulated by cellular antioxidant enzymes, such as superoxide dismutases, catalase, glutathione peroxidases and peroxiredoxins. Therapeutic approach targeting these antioxidant enzymes might prove beneficial for prevention of ROS-related atherosclerotic vascular disease. Conversely, the development of specific antioxidant enzyme-mimetics could contribute to the clinical effectiveness.

• Toxicological Research
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• v.11 no.1
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• pp.161-168
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• 1995

It has been found that various stress challenges induce the myocardial antioxidant enzymes and produce an acquisition of the cellular resistance to the ischemic injury in animal hearts. Most of the stresses, however, seem to be guite dangerous to an animal's life. In the present study, therefore, we tried to search for safely applicable stress modalities which could lead to the induction of antioxidant enzymes and the production of myocardial tolerance to the ischemia-reperfusion injury. Male Sprague-Dawley rats (200-250 g) were exposed to various non-fatal stress conditions, i.e., hyperthermia (environmental temperature of $42^{\circ}C$ for 30 min, non-anesthetized animal), iramobilization (60 min), treadmill exercise (20 m/min, 30min), swimming (30 min), and hyperbaric oxyflenation (3 atm, 60 min), once a day for 5 days. The activities of myocardial antioxidant enzymes and the ischemia-reperfusion injury of isolated hearts were evaluated at 24 hr after the last application of the stresses. The activities of antioxidant enzymes, superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase (G6PD), were assayed in the freshly excised ventricular tissues. The ischemia-reperfusion injury was produced by 20 min-global ischemia followed by 30 min-reperfusion using a Langendorff perfusion system. In swimming and hyperbaric oxygenation groups, the activities of SOD and G6PD increased significantly and in the hyperthermia group, the catalase activity was elevated by 63% compared to the control. The percentile recoveries of cardiac function at 30 min of the post-ischemic reperfusion were 55.4%, 73.4%, and 74.2% in swimming, the hyperbaric oxygenation and the hyperthermia groups, respectively. The values were significantly higher than that of the control (38.6%). In additions, left ventricular end-diastolic pressure and lactate dehydrogenase release were significantly reduced in the stress groups. The results suggest that the antioxidant enzymes in the heart could be induced by the apparently safe in vivo-stresses and this may be involved in the myocardial protection from the ischemia-reperfusion injury.

• BMB Reports
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• v.37 no.5
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• pp.618-624
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• 2004

All members of R. glutinosa show the unique characteristic of intrinsic tolerance to paraquat (PQ). Antioxidant enzymes have been proposed to be the primary mechanism of PQ resistance in several plant species. Therefore, the antioxidant enzyme systems of R. glutinosa were evaluated by comparatively analyzing cellular antioxidant enzyme levels, and their responses of oxidative stresses and hormones. The levels of ascorbate peroxidase (APX), glutathione reductase (GR), non-specific peroxidase (POX), and superoxide dismutase (SOD) were 7.3-, 4.9-, 2.7- and 1.6-fold higher in PQ-tolerant R. glutinosa than in PQ-susceptible soybeans. However, the activity of catalase (CAT) was about 12-fold higher in the soybeans. The activities of antioxidant enzymes reduced after PQ treatment in the two species, with the exception of POX and SOD in R. glutinosa, which increased by about 40%. Interestingly, the activities of APX, SOD and POX in R. glutinosa, relative to those in soybeans, were further increased by 49, 67 and 93% after PQ treatment. The considerably higher intrinsic levels, and increases in the relative activities of antioxidant enzymes in R. glutinosa under oxidative stress support the possible role of these enzymes in the PQ tolerance of R. glutinosa. However, the relatively lower levels of SOD versus PQ tolerance, and the mixed responses of antioxidant enzymes to stresses and hormones, suggest a possible alternative mechanism(s) for PQ tolerance in R. glutinosa.

• Preventive Nutrition and Food Science
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• v.21 no.1
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• pp.24-30
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• 2016

Fresh ginseng roots were aged in an oven at $80^{\circ}C$ for 14 d. The in vitro and in vivo antioxidant activities of this aged ginseng, in comparison with those of the white and red ginsengs, were evaluated. In in vitro antioxidant assays, the ethanolic extracts from aged ginseng showed significantly higher free radical scavenging activity and reducing power than those of the white and red ginsengs. In in vivo antioxidant assays, mice were fed a high fat diet supplemented with white, red, or aged ginseng powders. High fat feeding resulted in a significant increase in lipid peroxidation and a substantial decrease in antioxidant enzymes activities in the animals. However, diet supplementation of ginseng powders, particularly aged ginseng, markedly reduced lipid peroxidation and enhanced the antioxidant enzymes activities. The results illustrate that the aged ginseng has greater in vitro and in vivo antioxidant capacity than the white and red ginsengs. The aged ginseng also showed considerably higher total saponin, phenolic, and flavonoid contents, indicating that its antioxidant capacity may have been partly due to its high levels of antioxidant compounds. This new ginseng product may be useful as a functional food with strong antioxidant potential.

• The Plant Pathology Journal
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• v.17 no.2
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• pp.88-93
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• 2001

Oxidative stress is one of the major limiting factor in plant productivity. Reactive oxygens species (ROS) generated during metabolic processes damage cellular functions and consequently lead to disease, senescence and cell death. Plants have evolved an efficient defense system by which the ROS is scavenged by antioxidant enzymes such as superoxide dismutase (SOD) and ascorbate peroxidase (APX). Attempts to reduce oxidative damages under the stress conditions have included the manipulation of 갠 scavenging enzymes by gene transfer technology. Increased SOD activities of transgenic plants lead to increased resistance against oxidative stresses derived from methyl viologen (MV), and from photooxidative damage caused by high light and low temperature. Transgenic tobacco plants overexpressing APX showed reduced damage following either MV treatment of photooxidative treatment. Overexpression of glutathion reductase (GR) leads to increase in pool of ascorbate and GSH, known as small antioxidant molecules. These results indicate through overexpression of enzymes involved in ROS-scavenging could maintain or improve the plant productivities under environment stress condition. In this study, the rational approaches to develop stress-tolerant plants by gene manipulation of antioxidant enzymes will be introduced to provide solutions for the global food and environmental problems in the $21^\textrm{st}$ century.

• Journal of Microbiology
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• v.39 no.2
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• pp.142-145
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• 2001

Changes in the Activities of several antioxidant enzymes in transformed human dermal microvascular endothelial Cells (HMEC-1) by infection with the obligate intracellular bacterium Orientia tsutsugamushi, the causative agent of scrub typhus, were investigated. The activities of glucose-6-phosphate dehydrogenase, catalase, and glutathione peroxidase were significantly decreased in HMEC-1 cells infected with Ο. tsutsugamushi. However, the level of superoxide dismutase increased slightly. Furthermore, Increased levels of intracellular peroxide was observed in HMEC-1 during infection. These results support the hypothesis that cells infected by this intracellular bacterium experience oxidant-mediated injury that may eventually contribute to cell death.

• Biomedical Science Letters
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• v.12 no.4
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• pp.427-433
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• 2006

We investigated the effect of propolis on the activity of antioxidant enzymes in rat liver exposed by X-ray irradiation. The dosage of propolis showed the effect of lowering the concentration of superoxide anion in irradiated rat liver, suggesting that propolis has a significant role to remove superoxide anion as an antioxidant and/or by activating the antioxidant enzyme. The activities of superoxide dismutase (SOD) and glutathione reductase (GR), disturbed by X-ray irradiation, were restored in 30 days to normal status in the group which dosed propolis before X-ray irradiation. Interestingly, catalase (CAT) and glutathione peroxidase (GPOX) activities were highly increased with feeding propolis to rat compared to untreated group, whereas glutathione s-transferase (GST) activity was little affected. Taken together, it suggests that the propolis has a protective role in the rat liver cells against X-ray irradiation by increasing and recovering the activities of antioxidant enzymes.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3663-3667
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• 2013

Background: Multiple myeloma is a malignant silent incurable plasma cell disorder. The present study aimed to assessed the activation of the oxidative stress pathway in afected patients Materials and Methods: Advanced oxidation protein products (AOPPs), malondialdehyde (MDA), adenosine deaminase (ADA), total antioxidant capacity (TAC) levels, glutathione, ascorbic acid (vitamin C), ${\alpha}$-tocopherol (vitamin E) in addition to related enzymes glutathione peroxidase (GSH-Px), glutathione reductase (GSH-R) and superoxide dismutase (SOD) were analyzed in sixty patients with multiple myeloma before and after one month treatment with induction therapy. Results: The results of the study showed a significant elevation in AOPPs, MDA, ADA levels in patients with multiple myeloma before and after treatment in comparison to healthy control samples In contrast TAC glutathione, vitamin C and E, and the antioxidant enzymes levels were decreased significantly. On comparing samples of MM patients after treatment, there was significant increase of TAC glutathione, vitamin C and E, and the antioxidant enzymes in parallel with decreasing AOPPs, MDA and ADA levels in comparison with samples of patients before treatment. Conclusions: The results indicate oxidative stress and DNA damage activity increase in MM and are alleviated in response to therapy.

• BMB Reports
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• v.48 no.4
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• pp.200-208
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• 2015

The field of redox proteomics focuses to a large extent on analyzing cysteine oxidation in proteins under different experimental conditions and states of diseases. The identification and localization of oxidized cysteines within the cellular milieu is critical for understanding the redox regulation of proteins under physiological and pathophysiological conditions, and it will in turn provide important information that are potentially useful for the development of novel strategies in the treatment and prevention of diseases associated with oxidative stress. Antioxidant enzymes that catalyze oxidation/reduction processes are able to serve as redox biomarkers in various human diseases, and they are key regulators controlling the redox state of functional proteins. Redox regulators with antioxidant properties related to active mediators, cellular organelles, and the surrounding environments are all connected within a network and are involved in diseases related to redox imbalance including cancer, ischemia/reperfusion injury, neurodegenerative diseases, as well as normal aging. In this review, we will briefly look at the selected aspects of oxidative thiol modification in antioxidant enzymes and thiol oxidation in proteins affected by redox control of antioxidant enzymes and their relation to disease. [BMB Reports 2015; 48(4): 200-208]