• The Korean Journal of Physiology and Pharmacology
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• 제8권6호
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• pp.339-344
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• 2004

Recent data have shown the importance of oxidative stresses in the pathogenesis of inflammatory bowel disease, crohn's disease and ulcerative colitis. $H_2O_2$, reactive oxygen species (ROS) donor, has been reported to act as a signaling molecule involved in a variety of cellular functions such as apo/ptosis and proliferation. In the present study, we investigated viability of cultured ileal smooth muscle cells (ISMC) after stimulation with $H_2O_2$. Trypan blue method revealed that the cell viability of ISMC treated with 1 mM $H_2O_2$ was not different from that of controls at up to 2 h time point, while treatment of ISMC with 1 mM $H_2O_2$ for 48 h finally induced significant decrease in the cell viability. Therefore, we evaluated whether $H_2O_2$ was capable of ERKs activation in ISMC for the short-term exposure and examined whether tyrosine kinase was involved in the process of ERK activation by $H_2O_2$ in ISMC. We also investigated the effects of $H_2O_2$ on activation of SAPK/JNK and p38 MAP kinase in ISMC. Thus, ISMC were cultured and exposed to $H_2O_2$, and western blot analysis was performed with phosphospecific MAP kinase antibodies. Robust activation of ERK occurred within 30 min of 1 mM $H_2O_2$ treatment. $H_2O_2-induced$ ERK activation was attenuated by a tyrosine kinase inhibitor, genistein, indicating that tyrosine kinase was probably involved in the ERK activation by $H_2O_2$. $H_2O_2$ was a moderate activator of SAPK/JNK, while p38 MAP kinase was not activated by $H_2O_2$. We suggest that ERK activation induced by short-term $H_2O_2$ treatment plays a critical role in cellular protection in the early stage of response to oxidative stress. The present study suggests the necessity of identification of MAPK signaling pathways affected by ROS, since it could ultimately elucidate cellular consequences involved in initiation and perpetuation of intestinal tissue damage in the diseases such as crohn's disease and ulcerative colitis, resulted from excessive ROS.

• Molecules and Cells
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• 제28권6호
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• pp.545-551
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• 2009

Mitogen-activated protein kinases (MAPK) affect the activation of activator protein-1 (AP-1), which plays an important role in regulating a range of cellular processes. However, the roles of these signaling factors on hydrogen peroxide ($H_2O_2$)-induced cell death are unclear. This study examined the effects of $H_2O_2$ on the activation of MAPK and AP-1 by exposing the cells to $H_2O_2$ generated by either glucose oxidase or a bolus addition. Exposing BJAB or Jurkat cells to $H_2O_2$ affected the activities of MAPK differently according to the method of $H_2O_2$ exposure. $H_2O_2$ increased the AP-1-DNA binding activity in these cells, where continuously generated $H_2O_2$ led to an increase in mainly the c-Fos, FosB and c-Jun proteins. The c-Jun-$NH_2$-terminal kinase (JNK)-mediated activation of c-Jun was shown to be related to the $H_2O_2$-induced cell death. However, the suppression of $H_2O_2$-induced oxidative stress by either JNK inhibitor or c-Jun specific antisense transfection was temporary in the cells exposed to glucose oxidase but not to a bolus $H_2O_2$. This was associated with the disruption of death signaling according to the severe and prolonged depletion of reduced glutathione. Overall, these results suggest that $H_2O_2$ may decide differently the mode of cell death by affecting the intracellular redox state of thiol-containing antioxidants, and this depends more closely on the duration exposed to $H_2O_2$ than the concentration of this agent.

• 한국진공학회:학술대회논문집
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• 한국진공학회 2011년도 제40회 동계학술대회 초록집
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• pp.333-333
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• 2011

We studied the H/D exchange kinetics of pure and acid dopped water-ice film by using the techniques of reactive ions scattering (RIS) and low energy sputtering (LES) with low kinetic energy cesium ion beam (<35 eV). From RIS, neutral water isotopomers were detected in the form of cesium-molecule ion clusters, $CsX^+$ (X= $H_2O$, HDO, $D_2O$). Ionic species, like $H_3O^+$, $DH_2O^+$, $D_2HO^+$, $D_3O^+$, adsorbed on the surface were ejected via LES process. Those techniques allowed us to trace the isotopomeric populations of water-ice film. To show the catalytic effect of excess proton in the H/D exchange reaction, our study was conducted with two types of water-ice films. In film 1, about 0.5 BL of $H_2O$ was adsorbed on HCl (0.1 ML) dopped $D_2O$ (8 BL) film. In film 2, similar amount of $H_2O$ used in film 1 was adsorbed on pure $D_2O$ film. Kinetic data were obtained from each film type for 90-110 K (film 1) and 110-130 K (film 2) and fitted with numerically integrated lines. Through the Arrhenius plot of kinetic coefficient deduced from fitting of the H/D exchange reaction, the activation energy of film 1 and 2 were estimated to be $10{\pm}3kJmol^{-1}$ and $17{\pm}4kJmol^{-1}$. This activation barrier difference could be understood from detailed pictures of H/D exchange. In film 2, both the formation of ion pair, $H_3O^+$ and OH. and proton transfer were needed for the H/D exchange. However, in film 1, only proton transfer was necessary but ion pair formation was not, so this might reduce the activation energy.

• 대한의생명과학회지
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• 제11권4호
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• pp.441-446
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• 2005

The molecular mechanism of ischemia/reperfusion injury remains unclear. Reactive oxygen species (ROS) are implicated in cell death caused by ischemia/reperfusion in vivo or hypoxia in vitro. Poly (ADP-ribose) polymerase (PARP) activation has been reported to be involved in hydrogen peroxide-induced cell death in renal epithelial cells. This study was therefore undertaken to evaluate the role of P ARP activation in chemical hypoxia in opossum kidney (OK) cells. Chemical hypoxia was induced by incubating cells with antimycin A, an inhibitor of mitochondrial electron transport. Exposure of OK cells to chemical hypoxia resulted in a time-dependent cell death. In OK cells subjected to chemical hypoxia, the generation of ROS was increased, and this increase was prevented by the $H_2O_2$ scavenger catalase. Chemical hypoxia increased P ARP activity and chemical hypoxia-induced cell death was prevented by the inhibitor of PARP activation 3-aminobenzamide. Catalase prevented OK cell death induced by chemical hypoxia. $H_2O_2$ caused PARP activation and $H_2O_2-induced$ cell death was prevented by 3-aminobenzamide. Taken together, these results indicate that chemical hypoxia-induced cell injury is mediated by PARP activation through H202 generation in renal epithelial cells.

• 한국재료학회지
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• 제13권1호
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• pp.31-35
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• 2003

The intensity is measured as functions of both distance from filament to substrate and $CH_3$OH/($CH_3$OH＋$H_2$O) ratio by OES(Optical Emission Spectroscopy) to investigate the effects of activation species such as $H_{\alpha}$, $H_{\beta}$, H$\Upsilon\;C_3$, CH on diamond film growth.$ H_{\alpha}$ increases as $CH_3$OH composition decreases, while CH increases as $CH_3$OH composition increases. The intensity of $H_{\alpha}$ decreases as the distance increases and that of CH increases as the distance increases. The intensities of other activation species of $H_{\beta}$, H$\Upsilon\;C_3$, do not vary as a function of measured position distance. It varies randomly. It means that various parameters for depositing diamond thin film can be explained by the intensity(density) change of activation species, as a function of the distance of the filament.

• Journal of Microbiology and Biotechnology
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• 제19권11호
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• pp.1355-1363
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• 2009

In the present study, the neuroprotective effects of astaxanthin on $H_2O_2$-mediated apoptotic cell death, using cultured mouse neural progenitor cells (mNPCs), were investigated. To cause apoptotic cell death, mNPCs were pretreated with astaxanthin for 8 h and followed by treatment of 0.3 mM $H_2O_2$. Pretreatment of mNPCs with astaxanthin significantly inhibited $H_2O_2$-mediated apoptosis and induced cell growth in a dose-dependent manner. In Western blot analysis, astaxanthin-pretreated cells showed the activation of p-Akt, p-MEK, p-ERK, and Bcl-2, and the reduction of p-P38, p-SAPK/JNK, Bax, p-GSK3b, cytochrome c, caspase-3, and PARP. Because $H_2O_2$ triggers caspases activation, this study examined whether astaxanthin can inhibit caspases activation in $H_2O_2$-treated mNPCs. After $H_2O_2$ treatment, caspases activities were prominently increased, but astaxanthin pretreatment significantly inhibited $H_2O_2$-mediated caspases activation. Astaxanthin pretreatment also significantly recovered the ATP production ability of $H_2O_2$-treated cells. These findings indicate that astaxanthin inhibits $H_2O_2$-mediated apoptotic features in mNPCs. Inhibition assays with SB203580 ($10\;{\mu}M$, a specific inhibitor of p38) and PD98059 ($10\;{\mu}M$, a specific inhibitor of MEK) clearly showed that astaxanthin can inhibit $H_2O_2$-mediated apoptotic death via modulation of p38 and MEK signaling pathways.

• 한국세라믹학회지
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• 제19권4호
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• pp.309-315
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• 1982

$FeAl_2O_4$ was formed from the starting material of $Fe_2O_3$ and $Al_2O_3$ by controlling the oxygen partial pressure using $H_2-CO_2$ gas mixture, over the temperature range of 800~120$0^{\circ}C$. The formation mechanism of $FeAl_2O_4$ was found to be a second order chemical reaction, and the activation energy of formation was observed as 39.97 kcal/mole. Vaporization behavior of $FeAl_2O_4$ under $CO_2$ atmosphere was observed over the temperature range of 800~120$0^{\circ}C$. $FeAl_2O_4$ was vaporized by a second order chemical reaction and the activation energy was found to be 21.8kcal/mole. Electrical conductivity of $FeAl_2O_4$ was also measured.

• The Korean Journal of Physiology and Pharmacology
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• 제25권1호
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• pp.51-58
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• 2021

Oxidative stress-induced neurodegeneration is one of several etiologies underlying neurodegenerative disease. In the present study, we investigated the functional role of histone methyltransferase G9a in oxidative stress-induced degeneration in human SH-SY5Y neuroblastoma cells. Cell viability significantly decreased on H2O2 treatment; however, treatment with the G9a inhibitor BIX01294 partially attenuated this effect. The expression of neuron-specific genes also decreased in H2O2-treated cells; however, it recovered on G9a inhibition. H2O2-treated cells showed high levels of H3K9me2 (histone H3 demethylated at the lysine 9 residue), which is produced by G9a activation; BIX01294 treatment reduced aberrant activation of G9a. H3K9me2 occupancy of the RE-1 site in neuron-specific genes was significantly increased in H2O2-treated cells, whereas it was decreased in BIX01294-treated cells. The differentiation of H2O2-treated cells also recovered on G9a inhibition by BIX01294. Consistent results were observed when used another G9a inhibitor UCN0321. These results demonstrate that oxidative stress induces aberrant activation of G9a, which disturbs the expression of neuron-specific genes and progressively mediates neuronal cell death. Moreover, a G9a inhibitor can lessen aberrant G9a activity and prevent neuronal damage. G9a inhibition may therefore contribute to the prevention of oxidative stress-induced neurodegeneration.

• 한국방사선학회논문지
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• 제7권3호
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• pp.213-219
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• 2013

현재 국내에서 가동 중인 싸이클로트론센터는 약 35개소에 이르며, 대부분의 싸이클로트론 센터는 주로 핵의학검사용 악성종양 추적자인 $^{18}FDG$ 등과 같은 방사성의약품을 생산하고 있다. 18F을 생산하기 위한 타겟으로서 산소동위원소비($^{18}O/O$)가 98%정도인 고농축 $H_2{^{18}}O$를 사용하고 있다. 고농축 $H_2{^{18}}O$는 1 gram당 가격이 약 60~70 USD 정도로 매우 고가이나 100% 수입에 의존하고 있는 상황이다. 양성자 빔 조사 전의 타겟(고농축 $H_2{^{18}}O$)은 비방사성이다. 하지만, "사용후 $H_2{^{18}}O$"는 불순물들의 방사화에 의해 방사능을 띄게 되므로 방사선안전 법규에 따라 적절한 관리가 이루어져야 한다. 최근의 핵의학검사 건수의 증가에 따라 사용 후 O-18의 발생량이 증가하고 있음에도 불구하고 국내에서는 현재까지 이에 대한 방사화분석이 이루어지지 않았다. 따라서, 본 연구에서는 $^{18}F$생산을 위해 양성자조사를 하고 난 타겟, 이른바 "사용후 O-18 water"의 방사화 분석을 실시하여 핵종별 방사능농도(Bq/g)를 확인하고자 하였다. 세 곳의 서로 다른 싸이클로트론 센터에서 보관 중인 "used $H_2{^{18}}O$" 중 20g 씩을 채취한 3개의 시료에 대해 방사화분석을 실시하였으며, 분석결과 사용후 O-18 water는 감마선 방출 방사성핵종인 $^{56}Co$, $^{57}Co$, $^{58}Co$, $^{54}Mn$ 등과 베타선 방출핵종인 $^3H$을 상당량 포함하고 있음을 확인할 수 있었다. 또한, 모든 시료에서 3H은 규제면제 농도 이하인 반면, 한 개 시료는 핵종별 규제면제농도 이상의 감마선 방출핵종을 포함하고 있음을 확인하였다. 시료에 포함된 감마선 방출핵종의 방사능 농도(Bq/g)는 조사 후 보관기간의 차이에 따라 달랐으며, 향후의 추가적인 연구가 더 필요하다고 판단되지만, 본 연구의 결과는 "사용후 O-18 water"의 합리적인 관리방안 수립을 위한 근거 자료로 활용될 수 있을 것이다.

• Biomolecules & Therapeutics
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• 제25권6호
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• pp.599-608
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• 2017

Tanshinone IIA (Tan IIA) is a pharmacologically active substance extracted from the rhizome of Salvia miltiorrhiza Bunge (also known as the Chinese herb Danshen), and is widely used to treat atherosclerosis. The pregnane X receptor (PXR) is a nuclear receptor that is a key regulator of xenobiotic and endobiotic detoxification. Tan IIA is an efficacious PXR agonist that has a potential protective effect on endothelial injuries induced by xenobiotics and endobiotics via PXR activation. Previously numerous studies have demonstrated the possible effects of Tan IIA on human umbilical vein endothelial cells, but the further mechanism for its exerts the protective effect is not well established. To study the protective effects of Tan IIA against hydrogen peroxide ($H_2O_2$) in human umbilical vein endothelial cells (HUVECs), we pretreated cells with or without different concentrations of Tan IIA for 24 h, then exposed the cells to $400{\mu}M$ $H_2O_2$ for another 3 h. Therefore, our data strongly suggests that Tan IIA may lead to increased regeneration of glutathione (GSH) from the glutathione disulfide (GSSG) produced during the GSH peroxidase-catalyzed decomposition of $H_2O_2$ in HUVECs, and the PXR plays a significant role in this process. Tan IIA may also exert protective effects against $H_2O_2$-induced apoptosis through the mitochondrial apoptosis pathway associated with the participation of PXR. Tan IIA protected HUVECs from inflammatory mediators triggered by $H_2O_2$ via PXR activation. In conclusion, Tan IIA protected HUVECs against $H_2O_2$-induced cell injury through PXR-dependent mechanisms.