• Title/Summary/Keyword: Tert-Butylhydroperoxide

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Changes in Biosynthesis of Glutathione and Taurine in Rat Liver Challenged with tert-Butylhydroperoxide (랫트 간에서 tert-Butylhydroperoxide 투여에 의한 글루타치온과 타우린의 생합성 변화)

  • Kim, Sun-Ju;Park, Hyun-Ah;Kim, Young-Chul
    • YAKHAK HOEJI
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    • v.53 no.6
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    • pp.314-320
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    • 2009
  • We examined metabolic conversion of cysteine into glutathione (GSH) and taurine in rat liver under oxidative stress. Administration of tert-butylhydroperoxide (t-BHP) into the portal vein of male rats resulted in a rapid elevation of serum sorbitol dehydrogenase, alanine aminotransferase, and aspartate aminotransferase activities, which decreased gradually in 24 hr. Hepatic cysteine concentration was reduced in 3 hr, and recovered progressively, reaching a level greater than 200% of the normal value in 24 hr. GSH was increased both in liver and blood at 9 hr after t-BHP challenge, whereas hypotaurine or taurine was not altered. $\gamma$-Glutamylcysteine synthetase (GCS) activity was increased from 9 hr after t-BHP treatment, but protein expression of the GCS-heavy subunit was not changed in liver. Activity or expression of cysteine dioxygenase was not affected by t-BHP treatment. Taken together, these data show that an acute oxidant challenge to the rats may induce upregulation of cysteine availability and GCS activity, resulting in an enhancement of hepatic GSH synthesis, but the increased cysteine level does not stimulate taurine synthesis via cysteine sulfinate pathway. It is indicated that the regulation of GSH and taurine biosynthesis from cysteine is not solely dependent on the cysteine concentration in rat liver under oxidative stress.

Phase equilibria and structure identification of tert-butylhydroperoxide + gaseous clathrate hydrates (이성분계(3차 부틸-히드로과산화물 + 기체) 클러스레이트 하이드레이트의 구조적 특성과 열역학적 안정성에 관한 연구)

  • Youn, Yeobeom;Cha, Minjun;Kwon, Minchul;Lee, Huen
    • 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.

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YS 49, a Synthetic Isoquinoline Alkaloid, Protects Sheep Pulmonary Artery Endothelial Cells from tert-butylhydroperoxide-mediated Cytotoxicity

  • Chong, Won-Seog;Kang, Sun-Young;Kang, Young-Jin;Park, Min-Kyu;Lee, Young-Soo;Kim, Hye-Jung;Seo, Han-Geuk;Lee, Jae-Heun;ChoiYun, Hye-Sook;Chang, Ki-Churl
    • The Korean Journal of Physiology and Pharmacology
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    • v.9 no.5
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    • pp.283-289
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    • 2005
  • Endothelium, particularly pulmonary endothelium, is predisposed to injury by reactive oxygen species (ROS) and their derivatives. Heme oxygenase (HO) has been demonstrated to provide cytoprotective effects in models of oxidant-induced cellular and tissue injuries. In the present study, we investigated the effects of YS 49 against oxidant [tert-butylhydroperoxide (TBH)]-induced injury using cultured sheep pulmonary artery endothelial cells (SPAECs). The viability of SPAECs was determined by quantifying reduction of a fluorogenic indicator Alamar blue. We found that TBH decreased cell viability in a timeand concentration-dependent manner. YS 49 concentration- and time-dependently increased HO-1 induction on SPAECs. As expected, YS 49 significantly decreased the TBH-induced cellular injury. In the presence of zinc protophorphyrin, HO-1 inhibitor, effect of YS 49 was significantly inhibited, indicating that HO-1 plays a protective role for YS 49. Furthermore, YS 49 showed free radical scavenging activity as evidenced by 1,1-diphenyl-2-picrylhydrazyl (DPPH) and inhibition of lipid peroxidation. However, YS 49 did not inhibit apoptosis induced by lipopolysaccharide (LPS) in SPAECs. Taken together, HO-1 induction along with strong antioxidant action of YS 49 may be responsible for inhibition of TBH-induced injury in SPAECs.

Protective Effect of Polysaccharide Fractions from Radix A. Sinensis against tert-Butylhydroperoxide Induced Oxidative Injury in Murine Peritoneal Macrophages

  • Yang, Xingbin;Zhao, Yan;Lv, You;Yang, Ying;Ruan, Yun
    • BMB Reports
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    • v.40 no.6
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    • pp.928-935
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    • 2007
  • Three Angelica sinensis polysaccharide fractions (APFs), named APF1, APF2 and APF3, were isolated and purified from Radix A. sinensis and their antioxidant activities were evaluated in isolated mouse peritoneal macrophages by pretreatment with APFs before exposure to 0.2 mM tertbutylhydroperoxide (t-BHP). The results showed that pretreatment of the macrophages with APFs as low as $10{\mu}g$/ml could significantly enhance t-BHP-decreased cell survival, intracellular glutathione (GSH) content and superoxide dismutase (SOD) activity, and also inhibited t-BHP-increased lactate dehydrogenase (LDH) leakage and malondialdehyde (MDA) formation (p < 0.05), and APF3 was the most active fraction, followed by APF2 and APF1 in decreasing order. Furthermore, we found for the first time that the bound-protein in APF3 was associated closely with the protective effects and the polysaccharide inhibited the excess NO release from t-BHP-activated macrophages to protect host cells.

Methods for Evaluation of Antioxidant Activity: Application to Taurine (항산화 활성의 평가를 위한 연구법: 타우린의 적용)

  • Kim, Bong-Hee;Oh, Jung-Min;Yun, Kang-Uk;Kim, Chung-Hyeon;Kim, Sang-Kyum
    • Toxicological Research
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    • v.23 no.3
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    • pp.263-269
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    • 2007
  • Although taurine (2-aminoethanesulfonic acid) can inhibit oxidative stress in both animal and epidemiological studies, it is obscure whether taurine directly scavenges oxy-radicals or indirectly regulates oxidant production and/or antioxidant defense system. The reason for this discrepancy remains unknown but may be due, in part, to the lack of a validated assay system for evaluating oxy-radical scavenging capacity. The antioxidant activities of taurine and hypotaurine (2-aminoethanesulfinic acid), a precursor of taurine, against peroxyl radicals, hydroxyl radicals and peroxynitrites were determined by the total oxy-radical scavenging capacity (TOSC) assay and cell-based assay using H4IIE cells. tert-Butylhydroperoxide or hydrogen peroxide-induced cell toxicity determined by MTT assay was markedly inhibited by 10mM taurine or hypotaurine. The tert-butylhydroperoxide- or hydrogen peroxide-induced changes in oxidative stress markers, such as cellular glutathione and malondialdehyde, were ameliorated by 10mM taurine or hypotaurine. However, specific TOSC values calculated from the slope of the linear regression for taurine against peroxyl radicals, hydroxyl radicals or peroxynitrites were all less than 1 TOSC/mM. On the other hand specific TOSC values for hypotaurine against peroxyl radicals, hydroxyl radicals or peroxynitrites were 48, 2096, or 69 TOSC/mM, respectively. These results suggest that taurine protects cells against oxidative insults, which is not ascribed to directly scavenging activity of taurine against oxy-radicals. These results support the idea that the oxidation state of sulfur in antioxidants may be a determinant of oxy-radical scavenging capacity.

The Mechanism of t-Butylhydroperoxide-Induced Apoptosis in IMR-32 Human Neuroblastoma Cells

  • Kim, Jung-Ae;Lee, Yong-Soo;Huh, Keun
    • 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.

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Characteristics of Oxidative Desulfurization(ODS) of Sulfur Compounds in Diesel Fuel over Ti-grafted SBA-15 Catalyst (Ti-grafted SBA-15 촉매를 이용한 경유유분 중의 황화합물의 선택산화탈황 특성)

  • Cho, Chin-Soo;Jeong, Kwang-Eun;Chae, Ho-Jeong;Kim, Chul-Ung;Jeong, Soon-Yong;Oh, Sung-Geun
    • 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.

Focus on Anti-Oxidative and Free Radical Scavenging Activity of Ganoderma lucidum

  • Lin, Zhi-Bin
    • Biomolecules & Therapeutics
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    • v.12 no.3
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    • pp.133-137
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    • 2004
  • Present review is built on base of research work on Ganoderma lucidum in our laboratory. A great deal of experimental evidence has suggested that the pharmacological activities of Ganoderma lucidum (Lingzhi) are related to anti-oxidative and free radical scavenging activity. The anti-oxidative and free radical scavenging effects of polysaccharides and triterpenoids isolated from Ganoderma lucidum in different oxidative injury models including tert-butylhydroperoxide (tBOOH)- damaged mice peritoneal macrophages, alloxan-induced diabetes, experimental liver injury models induced by carbon tetrachloride (CCl4), D-galactosamine (DGal) and Bacillus Calmette-Guerin (BCG) plus lipopolysaccharides (LPS) were investigated. It is also demonstrated that Lugu lingzhi, one of Ganoderma product, significantly inhibited LDL oxidation mediated by endothelial cells and decreased monocyte adhesion to endothelial cell (EC) induced by Oxidative low-density lipoprotein (ox-LDL) and advanced glycation endproducts (AGE). Lugulingzhi-treated serum could markedly inhibit the expression of intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-l) induced by ox-LDL and AGE.

Focus on anti-oxidative and free radical scavenging activity of Ganoderma lucidum

  • Lin, Zhi-Bin
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 2004.04a
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    • pp.61-77
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    • 2004
  • Present review is built on base of research work on Ganoderma lucidum in our laboratory. A great deal of experimental evidence has suggested that the pharmacological activities of Ganoderma lucidum(Lingzhi) are related to anti-oxidative and free radical scavenging activity. The anti-oxidative and free radical scavenging effects of polysaccharides and triterpenoids isolated from Ganoderma lucidum in different oxidative injury models including tert-butylhydroperoxide (tBOOH)- damaged mice peritoneal macrophages, alloxan-induced diabetes, experimental liver injury models induced by carbon tetrachloride (CC14), D-galactosamine (DGal) and Bacillus Calmette-Guerin(BCG) plus lipopolysaccharides(LPS) were investigated. It is also demonstrated that Lugu lingzhi, one of Ganoderma product, significantly inhibited LDL oxidation mediated by endothelial cells and decreased monocyte adhesion to endothelial cell (EC) induced by Oxidative low-density lipoprotein (ox-LDL) and advanced glycation endproducts(AGE). Lugulingzhi-treated serum could markedly inhibit the expression of intercellular cell adhesion molecule-l (ICAM-1) and vascular cell adhesion molecule-l (VCAM-1) induced by ox-LDL and AGE.

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Selective Oxidation of Olefins Catalyzed by Polymer-anchored Nickel(II) Complex in Water Medium

  • Islam, Manirul;Hossain, Dildar;Mondal, Paramita;Roy, Anupam Singha;Mondal, Sanchita;Mobarak, Manir
    • 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.