• Elastomers and Composites
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• v.38 no.2
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• pp.147-156
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• 2003

Synthesis of fullerene oxides by fullerenes [$C_{60},\;C_{70}$] and several oxidants such as benzoylperoxide, trichloroisocyanuric acid, methyltrioxorhenium(VII), iodosobenzene, phosphorous pentoxide take place under ultrasonic condition at room temperature. The MALDI-TOF MS,UV-visible spectra and HPLC analysis confirmed that the products of fullerenes oxidation are [$C_{60}(O)_n$], ($n=1{\sim}3$ or n=1) and [$C_{70}(O)_n$], ($n=1{\sim}2$ or n=1). As compared with the reactivity of epoxidation of fullerenes [$C_{60},\;C_{70}$], the reaction rate of $C_{70}$ was lower than that of $C_{60}$ under same reaction condition.

• Elastomers and Composites
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• v.40 no.1
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• pp.45-52
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• 2005

Synthesis or fullerene oxides[$C_{60}(O)_n$] ($n=1{\sim}4$ or n=1) by fullerene[$C_{60}$] and several oxidants such as 3-chloroperoxy benzoic acid, benzoyl peroxide, trichloroisocyanuric acid, and chromium(VI) oxide took place under microwave irradiation. The reactivity in solid state of fullerene[$C_{60}$] with various oxidants under same microwave rendition increased in order or 3- chloroperoxy benzoic acid > benzoyl peroxide > trichloroisocyanuric acid $\simeq$chromium(VI) oxide. The MALDI-TOF-MS, UV-visible spectra and HPLC analysis confirmed that the products of fullerene oxidation were [$C_{60}(O)_n$] ($n=1{\sim}4$ or n=1).

• Environmental Engineering Research
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• v.20 no.3
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• pp.205-211
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• 2015

Reduced forms of iron, such as zero-valent ion (ZVI) and ferrous ion (Fe[II]), can activate dissolved oxygen in water into reactive oxidants capable of oxidative water treatment. The corrosion of ZVI (or the oxidation of (Fe[II]) forms a hydrogen peroxide ($H_2O_2$) intermediate and the subsequent Fenton reaction generates reactive oxidants such as hydroxyl radical ($^{\bullet}OH$) and ferryl ion (Fe[IV]). However, the production of reactive oxidants is limited by multiple factors that restrict the electron transfer from iron to oxygen or that lead the reaction of $H_2O_2$ to undesired pathways. Several efforts have been made to enhance the production of reactive oxidants by iron-induced oxygen activation, such as the use of iron-chelating agents, electron-shuttles, and surface modification on ZVI. This article reviews the chemistry of oxygen activation by ZVI and Fe(II) and its application in oxidative degradation of organic contaminants. Also discussed are the issues which require further investigation to better understand the chemistry and develop practical environmental technologies.

• Elastomers and Composites
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• v.39 no.4
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• pp.309-317
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• 2004

Synthesis of fullerene oxides [$C_{70}O_n$] ($n=1{\sim}3$ or n=1) in solid state by fullerene [$C_{70}$] and several oxidants such as 3-chloroperoxy benzoic acid, chromium(VI) oxide, benzoyl peroxide, and trichloroisocyanuric acid was taken place under microwave irradiation. The reactivity in solid state oi fullerene [$C_{70}$] with various oxidants under same microwave condition increased in the order of 3-chloroperoxy benzoic acid > chromium(VI) oxide > trichloroisocyanuric acid ${\simeq}benzoyl$ peroxide. The MALDI-TOF-MS, UV-visible spectra and HPLC analysis confirmed that the products of fullerene oxidation were [$C_{70}O_n$] ($n=1{\sim}3$ or n=1).

• The Journal of Korean Medicine
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• v.17 no.1 s.31
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• pp.9-20
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• 1996

Oxygen free radicals can generated during metabolic processes in normal cells and by exposure of cells to toxic substances. These radicals have been recogenized to playa critical role in several pathological conditions including carcinogenesis and aging, and they have been implicated in pathogenesis of various diseases such as seizure, Alzheimer's disease, Parkinson's disease, myocardial infarction, respiratory distress syndrome, and rheumatoid arthritis. This study was undertaken to determine if Juglandis semen herb-acupuncture solution (JSHAS) has a protective effect against cell injury caused by oxidants, t-butylhydroperoxide (t-BHP) and $H_{2}O_2$. Cell injury was estimated by measuring lactate dehydrogenase (LDH) release and lipid perexidation was estimated by measurimg malondialdehyde, a product of lipid peroxidation. JSHAS significantly prevented LDH release induced by t-BHP or $H_{2}O_2$ in a dose-dependent manner at concentrations of 0.5-10%. Such protective effect was observed in control tissues untreated with oxidants. JSHAS, at 5% concentration, significantly reduced LDH release even when the concentrations of t-BHP and $H_{2}O_2$ increased to 5 and 200 mM, respectively. JSHAS, at 5% concentration, significantly reduced the lipid peroxidation by t-BHP and $H_{2}O_2$. These results indicate that JSHAS prevents cell injury and lipid peroxidation induced by oxidants in rabbit kidney cells. However, the underlying mechanisms remain to determined.

• The Transactions of the Korean Institute of Electrical Engineers C
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• v.50 no.2
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• pp.79-85
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• 2001

A conventional electrolyzing cell has been made by an ion exchange membrane inbetween parallel plate electrodes. A low dc voltage is applied to the electrodes for electrolyzing and the efficiency is remained in low. in this study, a novel electrolyzing cell with a pair of slit-type third electrodes installed inbetween parallel plate electrodes has been proposed and investigated experimentally. And pulse power wa supplied to between each electrodes. This slit type of third electrodes can concentrate the strong electric fields at the every its edges to accelerate the electrolyzing powers, and to generate oxygen bubble discharges for generating oxidants. And moreover the slits eliminate the space charge limiting action and the temperature of the water by leaking out through the slits from electrolyzing region to outside of the main electrode region. As a result, it was found that a strong electorzed water of pH 2.8 and pH 10.5 and oxidants dissolved water of 1 [ppm] in acidic water were obtained with a tap water fed at the electric current of 2 [A], which however were several times higher oxidant and ion concentration quantity compared with the conventional cell.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.11
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• pp.4405-4409
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• 2014

Reactive oxygen species (ROS), highly reactive molecules, are produced by living organisms as a result of normal cellular metabolism and environmental factors, and can damage nucleic acids and proteins, thereby altering their functions. The human body has several mechanisms to counteract oxidative stress by producing antioxidants. A shift in the balance between oxidants and antioxidants in favor of oxidants is termed as "oxidative stress". Paradoxically, there is a large body of research demonstrating the general effect of oxidative stress on signaling pathways, less is known about the initial and direct regulation of signaling molecules by ROS, or what we term the "oxidative interface." This review focuses on the molecular mechanisms through which ROS directly interact with critical signaling molecules to initiate signaling in a broad variety of cellular processes, such as proliferation and survival (MAP kinases and PI3 kinase), ROS homeostasis, and antioxidant gene regulation (Ref-1 and Nrf-2). This review also deals with classification as well as mechanisms of formation of free radicals, examining their beneficial and deleterious effects on cellular activities and focusing on the potential role of antioxidants in preventing and repairing damage caused by oxidative stress. A discussion of the role of phytochemical antioxidants in oxidative stress, disease and the epigenome is included.

• BMB Reports
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• v.36 no.1
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• pp.95-109
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• 2003

Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance. The sources of the increased oxidative stress in patients with chronic inflammatory lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and various structural cells of the airways. Increased levels of ROS produced in the airways is reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with lung diseases. ROS, either directly or via the formation of lipid peroxidation products such as 4-hydroxy-2-nonenal may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38) and redox sensitive transcription factors such as NF-${\kappa}B$ and AP-1. Recent evidences have indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Understanding of the mechanisms of redox signaling, NF-${\kappa}B$/AP-1 regulation, the balance between histone acetylation and deacetylation and the release and expression of pro- and anti-inflammatory mediators may lead to the development of novel therapies based on the pharmacological manipulation of antioxidants in lung inflammation and injury. Antioxidants that have effective wide spectrum activity and good bioavailability, thiols or molecules which have dual antioxidant and anti-inflammatory activity, may be potential therapeutic agents which not only protect against the direct injurious effects of oxidants, but may fundamentally alter the underlying inflammatory processes which play an important role in the pathogenesis of chronic inflammatory lung diseases.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.50 no.6
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• pp.684-693
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• 2017

We investigated methods for extracting histidine-containing low-molecular-weight (LMW) peptides such as anserine, carnosine and histidine from the edible meat of tuna byproducts. Extracts were treated by several methods including heat treatment ($80^{\circ}C$, 10 min), DOWEX ion exchange (IEC), ultrafiltration (UF), and carboxymethyl (CM)-cellulose column chromatography (IEC+CMC); then the levels of protein, total iron, histidine, carnosine, and anserine were measured. Extracts treated with IEC+CMC using CM-cellulose were analyzed for total iron, protein, histidine, and anserine content, which were $6.27{\pm}0.26mg/mL$, $5.20{\pm}0.21{\mu}g/mL$, 0.80 mg/mL, 0.208 mg/mL, and 4.40 mg/mL, respectively, in yellowfin tuna; and $9.05{\pm}0.82mg/mL$, $4.06{\pm}0.20{\mu}g/mL$, 1.62 mg/mL, 0.012 mg/mL, and 7.28 mg/mL in bigeye tuna. By comparison in IEC-UF treated extracts, protein, total iron, and histidine content decreased by 43%, 73%, and 27% in yellowfin and 0.4%, 54%, and 23% in bigeye tuna, wheres carnosine and anserine content increased by 22% and 17%, respectively. Freeze-dried (FD) extracts exhibited similar trends as non-dried extracts, i.e., dipeptide content increased with purification steps, whereas pro-oxidant (total iron and protein) content decreased. IEC+CMC treated FD extracts had the highest anserine, content, and the greatest reductuion in pro-oxidants.

• The Journal of Korean Obstetrics and Gynecology
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• v.19 no.1
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• pp.97-110
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• 2006

Purpose : To address the ability of Myrrha (MY) to induce cell death, we investigated the effect of MY on apoptosis. In human cervical carcinoma HeLa cells, apoptosis occurred following MY exposure in a dose-dependent manner. Methods : We have tested several kinds of anti-oxidants to investigate the MY-induced apoptotic mechanism. Among the anti-oxidants, N-acetyl cysteine(NAC) or reduced glutathione (GSH) protects MY-induced apoptosis. NAC is an aminothiol and synthetic precursor of intracellular cysteine and GSH. To confirm the role of GSH in MY-induced apoptosis, methionine and cystathionine-glutathione extrusion inhibitors were treated in the presence of MY. Results : NAC, GSH, methionine or cystathionine led to protective effect against MY-induced apoptosis in HeLa cells. The GSH and GSH-associated reagents regulate MY-induced cytochrome c release and the resultant caspase-3 activation. Furthermore, the two specific inhibitors of carrier-mediated GSH extrusion, methionine and cystathionine demonstrate GSH extrusion occurs via a specific mechanism. While decreasing GSH extrusion and protecting against MY-induced apoptosis, methionine and cystathionine failed to exert anti-apoptotic activity in cells previously deprived of GSH. Conclusion : the target of the protection is indeed GSH extrusion. This shows that the protective effect is achieved by forcing GSH to stay within the cells during apoptogenic treatment. All this evidence indicates the extrusion of GSH precedes andis responsible for the apoptosis, probably by altering the intracellular redox state, thus giving a rationale for the development of redox-dependent apoptosis in MY-treated human cervical carcinoma HeLa cells.