• Journal of the Korean Chemical Society
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• v.66 no.3
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• pp.209-217
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• 2022

We have developed photosensitive electrochromic smart windows that does not require any transparent conducting oxide (TCO) substrate. In our previous study, we demonstrated that a flexible film-type device made with a low temperature curing WO₃ sol and TiO₂ sol could show a reversible and rapid switching between colored and bleached state via incorporation of platinum catalysts on the surface of WO₃ layer. However, when these devices were exposed to sunlight over 4 hour, it was confirmed that they did not return to fully bleached state in the darkened state due to their overcoloring process. In this study, we added 4-hydroxy-(2,2,6,6-tetramethylpiperidin-1-yl)oxyl (TEMPOL) as an additive to the electrolyte of photosensitive electrochromic device to effectively prevent the undesired overcoloring process. The resulting device with TEMPOL indeed did not undergo excessive coloration and showed great reversibility even after being exposed to sunlight for over 4 hours. Various concentrations of TEMPOL were applied to compare changes in the visible transmittance and coloring/bleaching kinetics of devices. In terms of energetic point of view, we proposed a plausible mechanism of TEMPOL to prevent excessive coloration.

• Yonsei Medical Journal
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• v.59 no.9
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• pp.1079-1087
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• 2018

Purpose: Obstructive sleep apnea and chronic obstructive pulmonary disease are independent risk factors of cardiovascular disease (CVD), and their coexistence is known as overlap syndrome (OS). Endothelial dysfunction is the initial stage of CVD; however, underlying mechanisms linking OS and CVD are not well understood. The aim of this study was to explore whether OS can lead to more severe inflammation and endothelial apoptosis by promoting endothelial dysfunction, and to assess the intervention effects of antioxidant tempol. Materials and Methods: Male Wistar rats (n=66) were exposed to normal oxygen [normal control (NC) group], intermittent hypoxia (IH group), cigarette smoke (CH group), as well as cigarette smoke and IH (OS group). Tempol intervention was assessed in OS group treated with tempol (OST group) or NaCl (OSN group). After an 8-week challenge, lung tissues, serum, and fresh blood were harvested for analysis of endothelial markers and apoptosis. Results: The levels of intracellular adhesion molecule-1, vascular cellular adhesion molecule-1, and apoptosis in circulating epithelial cells were the highest in OS group and the lowest in NC group. These levels were all greater in IH group than in CH group, and were lower in OST group than in OS and OSN groups (all p<0.001). Conclusion: Synergistic effects of IH with cigarette smoke-induced emphysema produce a greater inflammatory status and endothelial apoptosis. OS-related inflammation and endothelial cell apoptosis may play important roles in promoting cardiovascular dysfunction, and antioxidant tempol could achieve a partial protective effect.

• Korean Chemical Engineering Research
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• v.57 no.6
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• pp.868-873
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• 2019

In this study, the evaluation of performance of AORFB using methyl viologen and TEMPOL as organic active materials in neutral supporting electrolyte (NaCl) with various membrane types was performed. Using methyl viologen and TEMPOL as active materials in neutral electrolyte solution, the cell voltage is 1.37V which is relatively high value for AORFB. Two types of membranes were examined for performance comparison. First, when using Nafion 117 membrane which is commercial cation exchange membrane, only the charge process occurred in the first cycle and the single cell couldn't work because of its high resistance. However, when using Fumasep anion exchange membrane (FAA-3-50) instead of Nafion 117 membrane, the result was obtained as the totally different charge-discharge graphs. When current density was $40mA{\cdot}cm^{-2}$ and cut off voltage range was from 0.55 V to 1.7 V, the charge efficiency (CE) was 97% and voltage efficiency (VE) was 78%. In addition, the discharge capacity was $1.44Ah{\cdot}L^{-1}$ which was 54% of theoretical capacity ($2.68Ah{\cdot}L^{-1}$) at $10^{th}$ cycle and the capacity loss rate was $0.0015Ah{\cdot}L^{-1}$ per cycle during 50 cycles. Through cyclic voltammetry test, it seems that this difference in the performance between the full cell using Nafion 117 membrane and Fumasep anion exchange membrane came from increasing resistance due to chemical reaction between membrane and active material, not the capacity loss due to cross-over of active material through membrane.

• Applied Chemistry for Engineering
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• v.2 no.4
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• pp.311-329
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• 1991

Electrochemical behavior of surface active Osmium bipyridine complex adsorbed in a monomolecular layer on tin oxide electrodes by the Langmuir-Blodgett method was studied. Theoretical equation of cyclic voltammetry of electrode reactions for redox species adsorbed as monolayer form was discussed by reversible and quasi-reversible waves. The film was transferred onto the $SnO_2$ electrode surface and then amounts of charge on the electrode were measured in the technique of cyclic voltammetry. The electron transfer mediation of these monolayer with $Fe^{2+}$, TEMPOL and others were studied. And the cyclic voltammetry were simulated by taking into account the interaction parameters. From these values, we found it possible to fit almost all measured cyclic voltammograms with these parameters. The recent works and directions using LB method were introduced with various applicable field.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.1
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• pp.27-32
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• 2009

The effects of oxidized low-density lipoprotein(OxLDL) and its major lipid constituent lysophosphatidylcholine(LPC) on $Ca^{2+}$ entry were investigated in cultured human umbilical endothelial cells(HUVECs) using fura-2 fluorescence and patch-clamp methods. OxLDL or LPC increased intracellular $Ca^{2+}$ concentration($[Ca^{2+}]_i$), and the increase of $[Ca^{2+}]_i$ by OxLDL or by LPC was inhibited by $La^{3+}$ or heparin. LPC failed to increase $[Ca^{2+}]_i$ in the presence of an antioxidant tempol. In addition, store-operated $Ca^{2+}$ entry(SOC), which was evoked by intracellular $Ca^{2+}$ store depletion in $Ca^{2+}$-free solution using the sarcoplasmic reticulum $Ca^{2+}$ pump blocker, 2, 5-di-t-butyl-l,4-benzohydroquinone(BHQ), was further enhanced by OxLDL or by LPC. Increased SOC by OxLDL or by LPC was inhibited by U73122. In voltage-clamped cells, OxLDL or LPC increased $[Ca^{2+}]_i$ and simultaneously activated non-selective cation(NSC) currents. LPC-induced NSC currents were inhibited by 2-APB, $La^{3+}$ or U73122, and NSC currents were not activated by LPC in the presence of tempol. Furthermore, in voltage-clamped HUVECs, OxLDL enhanced SOC and evoked outward currents simultaneously. Clamping intracellular $Ca^{2+}$ to 1 ${\mu}M$ activated large-conductance $Ca^{2+}$-activated $K^+(BK_{ca})$ current spontaneously, and this activated $BK_{ca}$ current was further enhanced by OxLDL or by LPC. From these results, we concluded that OxLDL or its main component LPC activates $Ca^{2+}$-permeable $Ca^{2+}$-activated NSC current and $BK_{ca}$ current simultaneously, thereby increasing SOC.

• Journal of Life Science
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• v.21 no.4
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• pp.486-493
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• 2011

Nitric oxide (NO) donors are a potent inducer of heme oxygenase-1 (HO-1). However, it is unclear whether or not HO-1 expression induced by NO donors is a direct consequence of NO released by NO donors. Here, we investigated the effects of NO donors on the expression of HO-1 in primary rat articular chondrocytes. NO donors (SIN-1, SNAP, and SNP) significantly induced the accumulation of HO-1 protein accompanied by an increase in HO-1 mRNA. NO donor-induced HO-1 expression exerted cytoprotection against NO and/or superoxide-induced cell death. Guanylate cyclase signaling was not associated with Nrf2 and HO-1 expression in NO donor-treated chondrocytes. Interestingly, NO scavenger carboxy-PTIO and SOD mimetic TEMPOL markedly inhibited NO donor-induced HO-1 expression in chondrocytes. In addition, NO donor-induced HO-1 expression was completely abrogated by the peroxynitrite scavenger MnTBAP. Since peroxynitrite can be physiologcally formed in the cell through reaction of NO with superoxide, we analyzed whether or not peroxynitrite could directly induce HO-1 expression in chondrocytes. Peroxynitrite treatment in chondrocytes evoked doseand time-dependent Nrf2 and HO-1 expression. These results indicate that HO-1 expression induced by NO donors in rat articular chondrocytes is due to NO-mediated peroxynitrite rather than NO.

• International Journal of Oral Biology
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• v.37 no.1
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• pp.17-23
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• 2012

Recent studies indicate that reactive oxygen species (ROS) are critically involved in persistent pain primarily through spinal mechanisms, and that mitochondria are the main source of ROS in the spinal dorsal horn. To investigate whether mitochondrial ROS can induce changes in membrane excitability on spinal substantia gelatonosa (SG) neurons, we examined the effects of mitochondrial electron transport complex (ETC) substrates and inhibitors on the membrane potential of SG neurons in spinal slices. Application of ETC inhibitors, rotenone or antimycin A, resulted in a slowly developing and slight membrane depolarization in SG neurons. Also, application of both malate, a complex I substrate, and succinate, a complex II substrate, caused reversible membrane depolarization and enhanced firing activity. Changes in membrane potential after malate exposure were more prominent than succinate exposure. When slices were pretreated with ROS scavengers such as phenyl-N-tert-buthylnitrone (PBN), catalase and 4- hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL), malate-induced depolarization was significantly decreased. Intracellular calcium above $100{\mu}M$ increased malateinduced depolarization, witch was suppressed by cyclosporin A, a mitochondrial permeability transition (MPT) inhibitor. These results suggest that enhanced production of spinal mitochondrial ROS can induce nociception through central sensitization.

• Molecules and Cells
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• v.26 no.1
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• pp.18-25
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• 2008

Arsenic trioxide (ATO) can affect many biological functions such as apoptosis and differentiation in various cells. We investigated the involvement of ROS and GSH in ATO-induced HeLa cell death using ROS scavengers, especially N-acetylcysteine (NAC). ATO increased intracellular ${O_2}^{{\cdot}-}$ levels and reduced intracellular GSH content. The ROS scavengers, Tempol, Tiron and Trimetazidine, did not significantly reduce levels of ROS or GSH depletion in ATO-treated HeLa cells. Nor did they reduce the apoptosis induced by ATO. In contrast, treatment with NAC reduced ROS levels and GSH depletion in the ATO-treated HeLa cells and prevented ATO-induced apoptosis. Treatment with exogenous SOD and catalase reduced the depletion of GSH content in ATO-treated cells. Catalase strongly protected the cells from ATO-induced apoptosis. In addition, treatment with SOD, catalase and NAC slightly inhibited the G1 phase accumulation induced by ATO. In conclusion, NAC protects HeLa cells from apoptosis induced by ATO by up-regulating intracellular GSH content and partially reducing the production of ${O_2}^{{\cdot}-}$.

• International Journal of Oral Biology
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• v.40 no.2
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• pp.103-109
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• 2015

Growing evidence suggests that mitochondrial reactive oxygen species (ROS) are involved in various pain states. This study was performed to investigate whether ROS-induced changes in neuronal excitability in trigeminal subnucleus caudalis are related to ROS generation in mitochondria. Confocal scanning laser microscopy was used to measure ROS-induced fluorescence intensity in live rat trigeminal caudalis slices. The ROS level increased during the perfusion of malate, a mitochondrial substrate, after loading of 2',7'-dichlorofluorescin diacetate ($H_2DCF-DA$), an indicator of the intracellular ROS; the ROS level recovered to the control condition after washout. When pre-treated with phenyl N-tert-butylnitrone (PBN) and 4-hydroxy-2,2,6,6-tetramethylpiperidene-1-oxyl (TEMPOL), malate-induced increase of ROS level was suppressed. To identify the direct relation between elevated ROS levels and mitochondria, we applied the malate after double-loading of $H_2DCF-DA$ and chloromethyl-X-rosamine (CMXRos; MitoTracker Red), which is a mitochondria-specific fluorescent probe. As a result, increase of both intracellular ROS and mitochondrial ROS were observed simultaneously. This study demonstrated that elevated ROS in trigeminal subnucleus caudalis neuron can be induced through mitochondrial-ROS pathway, primarily by the leakage of ROS from the mitochondrial electron transport chain.

• Journal of Ginseng Research
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• v.47 no.1
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• pp.144-154
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• 2023

Background: As the major pathophysiological feature of obstructive sleep apnea (OSA), chronic intermittent hypoxia (CIH) is vital for the occurrence of cardiovascular complications. The activation of calpain-1 mediates the production of endothelial reactive oxygen species (ROS) and impairs nitric oxide (NO) bioavailability, resulting in vascular endothelial dysfunction (VED). Ginsenoside Rg1 is thought to against endothelial cell dysfunction, but the potential mechanism of CIH-induced VED remains unclear. Methods: C57BL/6 mice and human coronary artery endothelial cells (HCAECs) were exposed to CIH following knockout or overexpression of calpain-1. The effect of ginsenoside Rg1 on VED, oxidative stress, mitochondrial dysfunction, and the expression levels of calpain-1, PP2A and p-eNOS were detected both in vivo and in vitro. Results: CIH promoted VED, oxidative stress and mitochondrial dysfunction accompanied by enhanced levels of calpain-1 and PP2A and reduced levels of p-eNOS in mice and cellular levels. Ginsenoside Rg1, calpain-1 knockout, OKA, NAC and TEMPOL treatment protected against CIH-induced VED, oxidative stress and mitochondrial dysfunction, which is likely concomitant with the downregulated protein expression of calpain-1 and PP2A and the upregulation of p-eNOS in mice and cellular levels. Calpain-1 overexpression increased the expression of PP2A, reduced the level of p-eNOS, and accelerated the occurrence and development of VED, oxidative stress and mitochondrial dysfunction in HCAECs exposed to CIH. Moreover, scavengers of O₂^·-, H₂O₂, complex I or mitoKATP abolished CIH-induced impairment in endothelial-dependent relaxation. Conclusion: Ginsenoside Rg1 may alleviate CIH-induced vascular endothelial dysfunction by suppressing the formation of mitochondrial reactive oxygen species through the calpain-1 pathway.