• Applied Chemistry for Engineering
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• v.3 no.4
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• pp.649-656
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• 1992

The synthesis of epichlorohydrin was carried out by the epoxidation of allyl chloride with tert-butyl hydroperoxide(TBHP) over silica supported molybdenum catalyst. Kinetic study was performed at $60-80^{\circ}C$ and 10 atm with the molar ratio of TBHP/Allyl chloride between 0.01 and 0.1 in a batch reactor. The epoxidation of allyl chloride was inhibited by tert-butyl alcohol and kinetic data could be represented by Michaelis-Meten type rate equation. The reaction mechanism could be explained by the combination of reversible adsorption of TBHP and tert-butyl alcohol accompanied by reaction of allyl chloride with TBHP adsorbed on $Mo/SiO_2$ catalyst.

• Proceedings of the Korea Information Processing Society Conference
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• 2021.11a
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• pp.663-665
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• 2021

이미지에 대한 정보를 식별하는 기술인 이미지 인식은 현재 무인 자동차의 자율주행, 안면 인식, 의료 등의 여러 산업 분야에 적용되어 활발히 사용되고 있다. 이 중에서 이미지 객체 인식을 활용하여, 단순히 세포를 인식하는 것에서 더 나아가 TBHP 처리 세포에 대해 용액의 투입량과 시간 등의 다양한 조건을 고려함으로써 하나의 이미지에 포함된 세포의 전체 생존율을 판단하여 구분해보고자 한다.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.1
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• pp.19-27
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• 1999

Apoptosis has been implicated in the pathophysiological mechanisms of various neurodegenerative diseases. In a variety of cell types, oxidative stress has been demonstrated to play an important role in the apoptotic cell death. However, the exact mechanism of oxidative stress-induced apoptosis in neuronal cells is not known. In this study, we induced oxidative stress in IMR-32 human neuroblastoma cells with tert- butylhydroperoxide (TBHP), which was confirmed by significantly reduced glutathione content and glutathione reductase activity, and increased glutathione peroxidase activity. TBHP induced decrease in cell viability and increase in DNA fragmentation, a hallmark of apoptosis, in a dose-dependent manner. TBHP also induced a sustained increase in intracellular $Ca^{2+}$ concentration, which was completely prevented either by EGTA, an extracellular $Ca^{2+}$ chelator or by flufenamic acid (FA), a non-selective cation channel (NSCC) blocker. These results indicate that the TBHP-induced intracellular $Ca^{2+}$ increase may be due to $Ca^{2+}$ influx through the activation of NSCCs. In addition, treatment with either an intracellular $Ca^{2+}$ chelator (BAPTA/AM) or FA significantly suppressed the TBHP-induced apoptosis. Moreover, TBHP increased the expression of p53 gene but decreased c-myc gene expression. Taken together, these results suggest that the oxidative stress-induced apoptosis in neuronal cells may be mediated through the activation of intracellular $Ca^{2+}$ signals and altered expression of p53 and c-myc.

• 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.

• 한국신재생에너지학회:학술대회논문집
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• 2011.05a
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• pp.150.1-150.1
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• 2011

Structure-II hydrate has been highlighted due to its higher gas storage capacity and favorable thermodynamic conditions. In this study, we introduce a new structure-II hydrate former, tert-butyl hydroperoxide (TBHP) and confirm the structural characteristics through High-Resolution Powder Diffraction (HRPD), $^{13}C$ solide-state NMR and Ramanspectroscopy. Here,we also investigated the thermodynamic stability of binary(TBHP+gaseous) clathrate hydrates. The experimental data were generated using an isochoric pressure-search method. The dissociation data for (TBHP +gaseous) clathrate hydrates are compared with the other hydrocarbon hydrate and pure gaseous hydrate.

• Nutrition Research and Practice
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• v.8 no.2
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• pp.125-131
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• 2014

BACKGROUND/OBJECTIVES: The objective of this study was to evaluate the protective effect of black rice extract (BRE) on tert-butyl hydroperoxide (TBHP)-induced oxidative injury in HepG2 cells. MATERIALS/METHODS: Methanolic extract from black rice was evaluated for the protective effect on TBHP-induced oxidative injury in HepG2 cells. Several biomarkers that modulate cell survival and death including reactive oxygen species (ROS), caspase-3 activity, and related cellular kinases were determined. RESULTS: TBHP induced cell death and apoptosis by a rapid increase in ROS generation and caspase-3 activity. Moreover, TBHP-induced oxidative stress resulted in a transient ERK1/2 activation and a sustained increase of JNK1/2 activation. While, BRE pretreatment protects the cells against oxidative stress by reducing cell death, caspase-3 activity, and ROS generation and also by preventing ERKs deactivation and the prolonged JNKs activation. Moreover, pretreatment of BRE increased the activation of ERKs and Akt which are pro-survival signal proteins. However, this effect was blunted in the presence of ERKs and Akt inhibitors. CONCLUSIONS: These results suggest that activation of ERKs and Akt pathway might be involved in the cytoprotective effect of BRE against oxidative stress. Our findings provide new insights into the cytoprotective effects and its possible mechanism of black rice against oxidative stress.

• Korean Chemical Engineering Research
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• v.46 no.5
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• pp.845-851
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• 2008

Oxidative desulfurizaton of model sulfur compounds and Industrial diesel fuel(LCO; Light Cycle Oil) over Ti-grafted SBA-15 catalyst was studied in a batch reactor with tert-Butyl Hydroperoxide(TBHP) as oxidant. Effects of Ti loading, TBHP/Sulfur mole ratio, reaction temperature on ODS activity and kinetic parameters were investigated. Ti-grafted SBA-15 catalyst showed higher sulfur removal activity in the oxidative desulfurization reaction of refractory sulfur compounds(DBT and 4, 6-DMDBT) and LCO, suggesting that Ti-grafted SBA-15 catalyst could be a good candidate for ODS catalyst.

• YAKHAK HOEJI
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• v.49 no.6
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• pp.443-448
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• 2005

Diosgenin (25 (R) - spirost-5-en-3$\beta$ -ol) was oxidized with 2,3-dichloro -5,6-dicyano-1,4-benzoquinone to form 25(R)-1,4,6-spirostatrien-3-one (1) as rigid cyclic $\alpha$,$\beta$-unsaturated carbonyl compound. This compound was reacted with $H_{2}O_{2}$, m-chloroperoxybenzoic acid (mCPBA), NaOCl in the presence with (R,R)- or (S,S)-Jacobsen catalyst, tert-butyl-hydroperoxide (TBHP) in Mo$(CO)_{6}$, and in VO $(acac)_{2}$ catalyst, respectively, 25(R) -1,4,6-spirostatrien -3-one (1) was reduced with $NaBH_{4}$ L-Selectride, $LiAIH_{4}$,$BH_{3}$ $\cdot$$(CH_{3})_{2}S$, Superhydride, Red-Al, and lithium tri-tert-butoxyaluminium hydride. And 25(R)-4,6-spirostadien-3$\beta$-ol (4) was treated with $H_{2}O_{2}$, mCPBA, TBHP in D - (-) - and L-(+)-diisopropyltar-trate and $Ti(OiPr)_{4}$ condition (Sharpless asymmetric epoxidation), TBHP in $Mo(CO)_{6}$, and in $VO(acac)_{2}$ catalyst, respectively.

• Bulletin of the Korean Chemical Society
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• v.31 no.12
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• pp.3765-3770
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• 2010

Selective oxidation of olefins has been carried out in water medium with tert-butylhydroperoxide (TBHP, 70% aqueous) as an oxidant using polymer-anchored Ni(II) complex as a catalyst. Several parameters were varied to optimize the reaction conditions. Under the optimized reaction conditions olefins gave selectively allylic oxidation products. The present polymer anchored Ni(II) complex can be recycled five times without any appreciable loss in catalytic activity.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.3
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• pp.181-187
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• 2013

Reactive oxygen species (ROS) are generated in various cells, including vascular smooth muscle and endothelial cells, and regulate ion channel functions. $K_{Ca}3.1$ plays an important role in endothelial functions. However, the effects of superoxide and hydrogen peroxide radicals on the expression of this ion channel in the endothelium remain unclear. In this study, we examined the effects of ROS donors on $K_{Ca}3.1$ expression and the $K^+$ current in primary cultured human umbilical vein endothelial cells (HUVECs). The hydrogen peroxide donor, tert-butyl hydroperoxide (TBHP), upregulated $K_{Ca}3.1$ expression, while the superoxide donors, xanthine/xanthine oxidase mixture (X/XO) and lysophosphatidylcholine (LPC), downregulated its expression, in a concentration-dependent manner. These ROS donor effects were prevented by antioxidants or superoxide dismustase. Phosphorylated extracellular signal-regulated kinase (pERK) was upregulated by TBHP and downregulated by X/XO. In addition, repressor element-1-silencing transcription factor (REST) was downregulated by TBHP, and upregulated by X/XO. Furthermore, $K_{Ca}3.1$ current, which was activated by clamping cells with 1 ${\mu}M$ $Ca^{2+}$ and applying the $K_{Ca}3.1$ activator 1-ethyl-2-benzimidazolinone, was further augmented by TBHP, and inhibited by X/XO. These effects were prevented by antioxidants. The results suggest that hydrogen peroxide increases $K_{Ca}3.1$ expression by upregulating pERK and downregulating REST, and augments the $K^+$ current. On the other hand, superoxide reduces $K_{Ca}3.1$ expression by downregulating pERK and upregulating REST, and inhibits the $K^+$ current. ROS thereby play a key role in both physiological and pathological processes in endothelial cells by regulating $K_{Ca}3.1$ and endothelial function.