• Bulletin of the Korean Chemical Society
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• v.17 no.10
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• pp.929-934
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• 1996

The electrochemistry and the reaction of non-μ-oxo dimer-forming [5,10,15,20-tetrakis(2,6-dichlorophenyl)porphyrinato] manganese(Ⅲ) chloride [(Cl8TPP)MnⅢCl] with tetraethylammonium hydroxide in water [-OH(H2O)] have been investigated by electrochemical and spectroscopic methods under anaerobic conditions. The stronger autoreduction of (C18TPP)MnⅢCl by -OH(H2O) in comparison with (Me12TPP)MnⅢCl by -OH(CH3OH) in MeCN is explained as the influence of electronic effects on substituted phenyl groups bonded to meso-position of porphyrin ring and the positive shift of reduction potential (-0.11 V) for (C18TPP)MnⅢCl. The autoreduction of manganese(Ⅲ) porphyrin to manganese (Ⅱ) by this process is only observed when one axial position is occupied by a ligating solvent and OH- coordinates the other axial site. The results are discussed in relation to the mechanisms for the reduction of manganese(Ⅲ) porphyrin.

• Bulletin of the Korean Chemical Society
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• v.33 no.12
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• pp.4015-4022
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• 2012

Manganese(III) 5-(4-carboxyphenyl)-10,15,20-triphenyl porphyrin chloride (Mn(TCPP)Cl) was grafted through amide bond on silica zeolite Y (HY), zeolite beta ($H{\beta}$) and hexagonal mesoporous silica (HMS). XRD, ICP-AES, $N_2$ physisorption, SEM, TEM, FTIR and thermal analysis were employed to analyse these novel heterogeneous materials. These silica supported catalysts were shown to be used for epoxidation and good shape selectivity was observed. The effect of support structure on catalytic performance was also discussed. The catalytic activity remained when the catalysts were recycled five times. The energy changes about epoxidation of alkenes by $NaIO_4$ and $H_2O_2$ were also computationally calculated to explain the different catalytic efficiency.

• Bulletin of the Korean Chemical Society
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• v.23 no.11
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• pp.1635-1639
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• 2002

A new solvent polymeric membrane sensor based on tetra(p-chlorophenyl)porphyrinato manganese (III) acetate is described which demonstrates excellent selectivity toward the triiodide ion. The electrode has a linear dynamic range between 1.0 ${\times}$ $10^{-2}$ M and 7.0 ${\times}$$10^{-6}$M with a Nernstian slope of $-59.6{\pm}1$ mV per decade and a detection limit of 5.0 ${\times}$$10^{-6}$M. The proposed sensor revealed good selectivities for triiodide over a wide variety of other anions and could be used in a pH range 2-9. The electrode can be used for at least two months without any considerable divergence in potential. It was applied as indicator electrode in potentiometric titration of the triiodide and As(III) ions.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.1
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• pp.25-36
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• 2022

To identify the effect and mechanism of carbon monoxide (CO) on delayed rectifier K⁺ currents (I_K) of human cardiac fibroblasts (HCFs), we used the wholecell mode patch-clamp technique. Application of CO delivered by carbon monoxidereleasing molecule-3 (CORM3) increased the amplitude of outward K⁺ currents, and diphenyl phosphine oxide-1 (a specific I_K blocker) inhibited the currents. CORM3-induced augmentation was blocked by pretreatment with nitric oxide synthase blockers (L-NG-monomethyl arginine citrate and L-NG-nitro arginine methyl ester). Pretreatment with KT5823 (a protein kinas G blocker), 1H-[1,-2,-4] oxadiazolo-[4,-3-a] quinoxalin-1-on (ODQ, a soluble guanylate cyclase blocker), KT5720 (a protein kinase A blocker), and SQ22536 (an adenylate cyclase blocker) blocked the CORM3 stimulating effect on I_K. In addition, pretreatment with SB239063 (a p38 mitogen-activated protein kinase [MAPK] blocker) and PD98059 (a p44/42 MAPK blocker) also blocked the CORM3's effect on the currents. When testing the involvement of S-nitrosylation, pretreatment of N-ethylmaleimide (a thiol-alkylating reagent) blocked CO-induced I_K activation and DL-dithiothreitol (a reducing agent) reversed this effect. Pretreatment with 5,10,15,20-tetrakis(1-methylpyridinium-4-yl)-21H,23H porphyrin manganese (III) pentachloride and manganese (III) tetrakis (4-benzoic acid) porphyrin chloride (superoxide dismutase mimetics), diphenyleneiodonium chloride (an NADPH oxidase blocker), or allopurinol (a xanthine oxidase blocker) also inhibited CO-induced I_K activation. These results suggest that CO enhances I_K in HCFs through the nitric oxide, phosphorylation by protein kinase G, protein kinase A, and MAPK, S-nitrosylation and reduction/oxidation (redox) signaling pathways.

• International Journal of Oral Biology
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• v.41 no.3
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• pp.141-147
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• 2016

Reactive oxygen species (ROS) and nitrogen species (RNS) are both important signaling molecules involved in pain transmission in the dorsal horn of the spinal cord. Xanthine oxidase (XO) is a well-known enzyme for the generation of superoxide anions ($O_2^{\bullet-}$), while S-nitroso-N-acetyl-DL-penicillamine (SNAP) is a representative nitric oxide (NO) donor. In this study, we used patch clamp recording in spinal slices of rats to investigate the effects of $O_2^{\bullet-}$ and NO on the excitability of substantia gelatinosa (SG) neurons. We also used confocal scanning laser microscopy to measure XO- and SNAP-induced ROS and RNS production in live slices. We observed that the ROS level increased during the perfusion of xanthine and xanthine oxidase (X/XO) compound and SNAP after the loading of 2',7'-dichlorofluorescin diacetate ($H_2DCF-DA$), which is an indicator of intracellular ROS and RNS. Application of ROS donors such as X/XO, ${\beta}-nicotinamide$ adenine dinucleotide phosphate (NADPH), and 3-morpholinosydnomimine (SIN-1) induced a membrane depolarization and inward currents. SNAP, an RNS donor, also induced membrane depolarization and inward currents. X/XO-induced inward currents were significantly decreased by pretreatment with phenyl N-tert-butylnitrone (PBN; nonspecific ROS and RNS scavenger) and manganese(III) tetrakis(4-benzoic acid) porphyrin (MnTBAP; superoxide dismutase mimetics). Nitro-L-arginine methyl ester (NAME; NO scavenger) also slightly decreased X/XO-induced inward currents, suggesting that X/XO-induced responses can be involved in the generation of peroxynitrite ($ONOO^-$). Our data suggest that elevated ROS, especially $O_2^{\bullet-}$, NO and $ONOO^-$, in the spinal cord can increase the excitability of the SG neurons related to pain transmission.