• Journal of Korean society of Dental Hygiene
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• v.21 no.5
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• pp.545-553
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• 2021

Objectives: This study aimed to investigate the cytotoxicity of Nexus RMGIC, an indirect restorative cement, on cell survival rate and reactive oxygen species (ROS) production in periodontal stem cells (PDSCs). Methods: PDSCs were incubated with serially diluted Nexus RMGIC eluates with and without the addition of N-acetyl-cysteine (NAC). Cell survival was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The ROS generation was determined by measuring the fluorescence intensity for 2',7'-dichlorofluorescin diacetate. Results: Nexus RMGIC exposure decreased cell proliferation and cell survival rate in a dose-dependent manner (1:8, 1:4, 1:2, 1:1) in PDSCs. The cytotoxicity of Nexus RMGIC was inhibited by treatment with 10-mM NAC. In addition, the production of ROS was detected by immunofluorescence after PDSCs were exposed to Nexus RMGIC. However, ROS generation was significantly suppressed in the NAC pretreatment compared with the Nexus RMGIC group. Conclusions: Nexus RMGIC increased the cytotoxicity and ROS generation. ROS was involved in Nexus RMGIC-induced cell toxicity.

• Journal of Applied Biological Chemistry
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• v.63 no.4
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• pp.457-462
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• 2020

Pancreatic cancer is among the most difficult-to-treat tumors. More than half of patients with this cancer have very few symptoms at the early stages, allowing the development of distant metastases and resistance to cancer treatment. In this study, we found that Juniperus chinensis extract (JCX) decreased the cell viability and migration activity of PANC-1 and SNU-213 pancreatic cancer cells in a dose-dependent manner. JCX increased caspase-3 activation and generation of reactive oxygen species (ROS). N-acetylcysteine treatment blocked JCX-induced ROS generation and the negative effects on pancreatic cancer cell viability. In addition, JCX down-regulated the levels of phospho-focal adhesion kinase (p-FAK) and phospho-extracellular signal-regulated kinase (p-ERK). Together, these results indicate that JCX induces apoptosis in human pancreatic cancer cell lines through ROS production, downregulating FAK/ERK signaling and activating caspase-3. We propose that JCX-derived compounds represent candidates for the development of alternative medicines for the treatment of pancreatic cancer.

• The Korean Journal of Pharmacology
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• v.21 no.1
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• pp.34-48
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• 1985

In vitro effects of nitrofurantoin, an antimicrobial agent for acute and chronic urinary tract infection, on the lung microsomal lipid peroxidation and the generation of reactive oxygen radicals were investigated to elucidate the biochemical mechanisms of its in vivopulmonary toxicity. The interaction of nitrofurantoin with porcine lung microsome resulted in significant lipid peroxidation. In addition, nitrofurantoin stimulated the generation of reactive oxygen radicals, $O^{-}_{2}{\cdot},\;H_2O_2$ as well as a highly reactive secondary oxygen species, $OH{\cdot}$. The stimulation of lipid peroxidation was inhibited not only by superoxide dismutase and catalase, but also by hydroxyl radical scavengers, mannitol and thiourea. Neither singlet oxygen $({^1}O_{2})$ was detected during the incubation of microsome with nitrofurantoin, nor lipid peroxidation was inhibited by singlet oxygen scavengers. When incubated anaerobically under the nitrogen atmosphere, the ability of nitrofurantoin to stimulatle lipid peroxidation was abolished. It appears that NADPH-dependent metaboliam of nitrofurantoin in pulmonary microsome under aerobic condition is accompanied by the stimulation of lipid peroxidation through the mediation of reactive oxygen radicals, particularly hydroxyl radical. It is strongly suggested from these results that the stimulation of pulmonary microsomal lipid peroxidation by the reactive oxygen radical may be a in vivo mechanism of pulmonary toxicity caused by nitrofurantoin.

• Journal of the Korean Society of Physical Medicine
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• v.1 no.1
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• pp.139-146
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• 2006

Purpose : This study is to understand the reactive oxygen which is expected to be a causative factor of aging condition including dementia, atherosclerosis, even cancer. Methods : The reactive oxygen is generated usually when people do very hard exercise or is under severe stressful situation or in unhealthy environment and as a protective reaction to reactive oxygen, human body releases antioxidant enzyme systems like superoxide dismutase (SOD), catalase, glutathione peroxidase (GPX), glutathion-S-transferase (GST) and non-enzymetic antioxidant systems like glutathione, ascorbate, $\beta$-carotene, vitimin E. Results : Nowadays, we are getting more interested in the generation of reactive oxygen especially in the area of physical education, food and nutrition, alternative medicine etc. Conclusion : The study of reactive oxygen in patients with musculoskeletal disease is also required and among various physical therapeutic approaches, the method of general coordinative manipulation is considered more necessary.

• Corrosion Science and Technology
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• v.5 no.3
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• pp.94-98
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• 2006

The next generation nuclear power reactor will use Pb-Bi as the cooling material. The steel structure materials such as HT-9 used in the reactor suffer from corrosion when they are exposed to high temperature Pb-Bi. Therefore corrosion should be prevented to use Pb-Bi as the coolant material without any safety problem. One method is to control the oxygen content in Pb-Bi. An appropriate amount of oxygen in Pb-Bi can produce a thin oxide layer on steel, and this layer protects the steel from corrosion attack. Since the required oxygen content in Pb-Bi is in the range of $10^{-5}$ to $10^{-7}$ wt%, this small oxygen content can be controlled by flowing a mixture of hydrogen gas and water vapor. The stagnant corrosion test of HT-9 samples was performed by controlling the oxygen content up to 2,000 hours. The corrosion behavior of HT-9 was analyzed at the temperatures of $500^{\circ}C$ and $650^{\circ}C$ with a reduced condition and a oxygen content of $10^{-6}$ wt%.

• 한국신재생에너지학회:학술대회논문집
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• 2008.10a
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• pp.51-54
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• 2008

This study aims to devise and analyze a power generation system combining the solid oxide fuel cell and oxy-fuel combustion technology. The fuel cell operates at an elevated pressure, a constituting a SOFC/gas turbine hybrid system. Oxygen is extracted from the high pressure cathode exit gas using ion transport membrane technology and supplied to the oxy-fuel power system. The entire system generates much more power than the fuel cell only system due to increased fuel cell voltage and power addition from oxy-fuel system. More than one third of the power comes out of the oxy-fuel system. The system efficiency is also higher than that of the fuel cell only system. Recovering most of the generated carbon dioxide is major advantage of the system.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.11a
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• pp.160-160
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• 2004

• Korean Journal of Materials Research
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• v.32 no.8
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• pp.339-344
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• 2022

The lattice oxygen mechanism (LOM) is considered one of the promising approaches to overcome the sluggish oxygen evolution reaction (OER), bypassing -OOH^* coordination with a high energetic barrier. Activated lattice oxygen can participate in the OER as a reactant and enables O^*-O^* coupling for direct O₂ formation. However, such reaction kinetics inevitably include the generation of oxygen vacancies, which leads to structural degradation, and eventually shortens the lifetime of catalysts. Here, we demonstrate that Se incorporation significantly enhances OER performance and the stability of NiFe (oxy)hydroxide (NiFe) which follows the LOM pathway. In Se introduced NiFe (NiFeSe), Se forms not only metal-Se bonding but also Se-oxygen bonding by replacing oxygen sites and metal sites, respectively. As a result, transition metals show reduced valence states while oxygen shows less reduced valence states (O^-/O₂^2-) which is a clear evidence of lattice oxygen activation. By virtue of its electronic structure modulation, NiFeSe shows enhanced OER activity and long-term stability with robust active lattice oxygen compared to NiFe.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.12
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• pp.4803-4812
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• 2015

Chronic alcohol and tobacco abuse plays a crucial role in the development of different liver associated disorders. Intake promotes the generation of reactive oxygen species within hepatic cells exposing their DNA to continuous oxidative stress which finally leads to DNA damage. However in response to such damage an entangled protective repair machinery comprising different repair proteins like ATM, ATR, H2AX, MRN complex becomes activated. Under abnormal conditions the excessive reactive oxygen species generation results in genetic predisposition of various genes (as ADH, ALDH, CYP2E1, GSTT1, GSTP1 and GSTM1) involved in xenobiotic metabolic pathways, associated with susceptibility to different liver related diseases such as fibrosis, cirrhosis and hepatocellular carcinoma. There is increasing evidence that the inflammatory process is inherently associated with many different cancer types, including hepatocellular carcinomas. The generated reactive oxygen species can also activate or repress epigenetic elements such as chromatin remodeling, non-coding RNAs (micro-RNAs), DNA (de) methylation and histone modification that affect gene expression, hence leading to various disorders. The present review provides comprehensive knowledge of different molecular mechanisms involved in gene polymorphism and their possible association with alcohol and tobacco consumption. The article also showcases the necessity of identifying novel diagnostic biomarkers for early cancer risk assessment among alcohol and tobacco users.

• Biomolecules & Therapeutics
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• v.21 no.3
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• pp.210-215
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• 2013

Ionizing radiation can induce cellular oxidative stress through the generation of reactive oxygen species, resulting in cell damage and cell death. The aim of this study was to determine whether the antioxidant effects of the flavonoid fisetin (3,7,3',4'-tetrahydroxyflavone) included the radioprotection of cells exposed to ${\gamma}$-irradiation. Fisetin reduced the levels of intracellular reactive oxygen species generated by ${\gamma}$-irradiation and thereby protected cells against ${\gamma}$-irradiation-induced membrane lipid peroxidation, DNA damage, and protein carbonylation. In addition, fisetin maintained the viability of irradiated cells by partially inhibiting ${\gamma}$-irradiation-induced apoptosis and restoring mitochondrial membrane potential. These effects suggest that the cellular protective effects of fisetin against ${\gamma}$-irradiation are mainly due to its inhibition of reactive oxygen species generation.