• Journal of the Korean Chemical Society
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• v.55 no.3
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• pp.463-471
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• 2011

A novel $N_2O_2$ Schiff base ligand, N,N'-bis(4-methoxysalicylidene)phenylendiamine(4-$CH_3O$-Salphen), has been synthesized. It has been revealed that the compound is very useful for the spectrophotometric quantification of Fe(II) and Fe(III) ions in aqueous solutions, such as mineral water, hot spring water, sea water, and waste water. The optimum conditions for the quantitative analysis are the followings; [4-$CH_3O$-Salphen]=$4.0{\times}10^{-4}\;M$, DMF/$H_2O$=70/30(v/v), pH=3.4~3.8, T= at $55^{\circ}C$, and prereaction time=1.0 hr. The sample of single valence state was prepared by the preliminary oxidation or reduction using $H_2O_2$ ($5.0{\times}10^{-4}\;M$) and $NH_2OH{\cdot}HCl$ ($5.0{\times}10^{-4}\;M$). The quantitative analyses of Fe(II) and Fe(III) ion were performed by measuring the absorbance at 434 nm and 456 nm, respectively. The estimated mean values agreed well with the standard values within the range of 2.00~6.90%. The limit of detection was 27.9 ng/mL for Fe(II) and 55.8 ng/mL for Fe(III).

• Journal of the Korean Chemical Society
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• v.38 no.2
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• pp.101-107
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• 1994

Some molybdenum(III) and (IV) complexes have been prepared from the reaction of $MoCl_4$·2MeCN with N, P, O-donating ligands and characterized by elemental analysis, infrared and UV-Visible spectroscopy. 3,5-Lutidine, 1,2-phenylenediamine, 8-hydroxyquinoline, 9,10-phenanthrenequinone, triphenylphosphine and 1,2-bis(diphenylphosphino)ethane were chosen as coordinating ligands. Stretching frequencies $\upsilon$ (Mo-Cl) of Mo(IV) appear at higher frequencies than those of Mo(III) complexes due to the increasing oxidation number of metal. $MoCl_4(L)_2$ exhibit one Mo-Cl stretching frequency, whereas Mo$Cl_4$(L^L) exhibit four Mo-Cl stretching frequencies. The number of Mo-Cl stretching frequency suggestes the former complexes have trans($D_{4h}$) and the latter complexes have cis($C_{2v}$) symmetry. Stretching frequency ${\nu}g(C{\equiv}N)$ of acetonitrile in Mo(III) complexes are shifted to about 30 $cm^{-1}$ higher frequency compared with that of a free ligand (2260 $cm^{-1}$). These spectral data indicates that Mo(III) complexes are in the octahedral geometries with the coordinated acetonitrile. Finally each molybdenum(III) and (IV) complexes showed the following formulation; $[MoCl_4(L)_2]$,[Mo$Cl_4$(L^L)], $[MoCl_3(L)_2MeCN]$ and [Mo$Cl_3$(L^L)MeCN].

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.109-113
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• 2001

Oxidized low-density lipoprotein (oxLDL) has been shown to modulate transactivations by the peroxisome proliferator activated receptor (PPAR)$\gamma$ and nuclear factor-kappa B (NF$\kappa$B). In this study, the oxLDL signaling pathways involved with the NF$\kappa$B transactivation were investigated by utilizing a reporter construct driven by three upstream NF$\kappa$B binding sites, and various pharmacological inhibitors. OxLDL and its constituent lysophophatidylcholine (lysoPC) induced a rapid and transient increase of intracellular calcium and stimulated the NF-KB transactivation in resting RAW264.7 macrophage cells in an oxidation-dependent manner. The NF$\kappa$B activation by oxLDL or lysoPC was inhibited by protein kinase C inhibitors or an intracellular calcium chelator. Tyrosine kinase or PI3 kinase inhibitors did not block the NF$\kappa$B transactivation. Furthermore, the oxLDL-induced NF$\kappa$B activity was abolished by the PPAR$\gamma$ ligands. When the endocytosis of oxLDL was blocked by cytochalasin B, the NF$\kappa$B transactivation by oxLDL was synergistically increased, while PPAR transactivation was blocked. These results suggest that oxLDL activates NF-$\kappa$B in resting macrophages via protein kinase C- and/or calcium-dependent pathways, which does not involve the endocytic processing of oxLDL. The endocytosis-dependent PPAR$\gamma$ activation by oxLDL may function as an inactivation route of the oxLDL induced NF$\kappa$B signal. Short heterodimer partner (SHP), specifically expressed in liver and a limited number of other tissues, is an unusual orphan nuclear receptor that lacks the conventional DNA-binding domain. In this work, we found that SHP expression is abundant in murine macrophage cell line RAW 264.7 but suppressed by oxLDL and its constituent I3-HODE, a ligand for peroxisome proliferator-activated receptor y. Furthermore, SHP acted as a transcription coactivator of nuclear factor-$\kappa$B (NF$\kappa$B) and was essential for the previously described NF$\kappa$B transactivation by lysoPC, one of the oxLDL constituents. Accordingly, NF$\kappa$B, transcriptionally active in the beginning, became progressively inert in oxLDL-treated RAW 264.7 cells, as oxLDL decreased the SHP expression. Thus, SHP appears to be an important modulatory component to regulate the transcriptional activities of NF$\kappa$B in oxLDL-treated, resting macrophage cells.

• Journal of Pharmacopuncture
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• v.18 no.2
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• pp.7-18
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• 2015

Objectives: Lawsone (1,4 naphthoquinone) is a non redox cycling compound that can be catalyzed by DT diaphorase (DTD) into 1,2,4-trihydroxynaphthalene (THN), which can generate reactive oxygen species by auto oxidation. The purpose of this study was to evaluate the toxicity of the phytomarker 1,4 naphthoquinone and its metabolite THN by using the molecular docking program AutoDock 4. Methods: The 3D structure of ligands such as hydrogen peroxide ($H_2O_2$), nitric oxide synthase (NOS), catalase (CAT), glutathione (GSH), glutathione reductase (GR), glucose 6-phosphate dehydrogenase (G6PDH) and nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) were drawn using hyperchem drawing tools and minimizing the energy of all pdb files with the help of hyperchem by $MM^+$ followed by a semi-empirical (PM3) method. The docking process was studied with ligand molecules to identify suitable dockings at protein binding sites through annealing and genetic simulation algorithms. The program auto dock tools (ADT) was released as an extension suite to the python molecular viewer used to prepare proteins and ligands. Grids centered on active sites were obtained with spacings of $54{\times}55{\times}56$, and a grid spacing of 0.503 was calculated. Comparisons of Global and Local Search Methods in Drug Docking were adopted to determine parameters; a maximum number of 250,000 energy evaluations, a maximum number of generations of 27,000, and mutation and crossover rates of 0.02 and 0.8 were used. The number of docking runs was set to 10. Results: Lawsone and THN can be considered to efficiently bind with NOS, CAT, GSH, GR, G6PDH and NADPH, which has been confirmed through hydrogen bond affinity with the respective amino acids. Conclusion: Naphthoquinone derivatives of lawsone, which can be metabolized into THN by a catalyst DTD, were examined. Lawsone and THN were found to be identically potent molecules for their affinities for selected proteins.

• Journal of Life Science
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• v.30 no.2
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• pp.211-220
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• 2020

The activity of CAR can be regulated not only by ligand binding but also by phosphorylation of regulatory factors involved in extracellular signaling pathways, cross-talk interactions with transcription factors, and the recruitment, degradation, and expression of coactivators and corepressors. This regulation of CAR activity can in turn have effects on the control of diverse physiological homeostasis, including xenobiotic and energy metabolism, cellular proliferation, and apoptosis. CAR is phosphorylated by the ERK1/2 signaling pathway, which causes formation of a complex with Hsp-90 and CCRP, leading to its cytoplasmic retention, whereas phenobarbital inhibits ERK1/2, which causes dephosphorylation of the downstream signaling molecules, leading to the recruitment to CAR of the activated RACK-1/PP2A components for the dephosphorylation, nuclear translocation, and the transcriptional activation of CAR. Activated CAR cross-talks with FoxO1 to induce inhibition of its transcriptional activity and with PGC-1α to induce protein degradation by ubiquitination, resulting in the transcriptional suppression of PEPCK and G6Pase involved in gluconeogenesis. Regulation by CAR of lipid synthesis and oxidation is achieved by its functional cross-talks, respectively, with PPARγ through the degradation of PGC-1α to inhibit expression of the lipogenic genes and with PPARα through either the suppression of CPT-1 expression or the interaction with PGC-1α each to induce tissue-specific inhibition or stimulation of β-oxidation. Whereas CAR stimulates cellular proliferation by suppressing p21 expression through the inhibition of FoxO1 transcriptional activity and inducing cyclin D1 expression, it suppresses apoptosis by inhibiting the activities of MKK7 and JNK-1 through the expression of GADD45B. In conclusion, CAR is involved in the maintenance of homeostasis by regulating not only xenobiotic metabolism but also energy metabolism, cellular proliferation, and apoptosis through diverse cross-talk interactions with extracellular signaling pathways and intracellular regulatory factors.