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Mingquan Yan - One of the best experts on this subject based on the ideXlab platform.
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Interpretation of the differential UV-visible absorbance spectra of metal-NOM complexes based on the quantum chemical simulations for the model compound Esculetin
Chemosphere, 2021Co-Authors: Chenyang Zhang, Xuze Han, Gregory V. Korshin, Andrey M. Kuznetsov, Mingquan YanAbstract:Abstract In this study, the model compound Esculetin that has functional groups typical for natural organic matter (NOM) was used to ascertain the nature of the characteristic bands in the differential UV-visible absorbance spectra (DAS) associated with the formation of metal-NOM complexes. The binding of ten different metal ions (Cu(II), Ni(II), Co(II), Fe(III), Cr(III), Al(III), Zn(II), Ca(II), Mg(II) and Pb(II)) with Esculetin generate four bands in the DAS. These bands are similar to those present in the DAS of metal-NOM complex. The UV-visible absorbance spectra of the metal-Esculetin systems were calculated using time-dependent density functional theory (TD-DFT). The TD-DFT results demonstrate that the prominent features of the DAS of Esculetin are primarily associated with the electron transitions between the molecular orbitals near the highest occupied molecular orbital (HOMO) and the lowest unoccupied molecular orbital (LUMO) in the metal-Esculetin complex. Charge decomposition analysis (CDA) results demonstrated that these electron transitions originate from the Esculetin fragment to the Zn(II) fragment in the complex. Covalent indexes [(χm)2rc] of the metal ions were found to be correlated with the metal-specific features of the DAS of metal-Esculetin systems. The strength of the linear correlations between the quantitative parameters of the electron density of the bond critical points (BCP) is indicative of the strength of the metal-Esculetin interactions.
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interpretation of the differential uv visible absorbance spectra of metal nom complexes based on the quantum chemical simulations for the model compound Esculetin
Chemosphere, 2021Co-Authors: Chenyang Zhang, Xuze Han, Gregory V. Korshin, Andrey M. Kuznetsov, Mingquan YanAbstract:In this study, the model compound Esculetin that has functional groups typical for natural organic matter (NOM) was used to ascertain the nature of the characteristic bands in the differential UV-visible absorbance spectra (DAS) associated with the formation of metal-NOM complexes. The binding of ten different metal ions (Cu(II), Ni(II), Co(II), Fe(III), Cr(III), Al(III), Zn(II), Ca(II), Mg(II) and Pb(II)) with Esculetin generate four bands in the DAS. These bands are similar to those present in the DAS of metal-NOM complexes. The UV-visible absorbance spectra of the metal-Esculetin systems were calculated using time-dependent density functional theory (TD-DFT). The TD-DFT results demonstrate that the prominent features of the DAS of Esculetin are primarily associated with the electron transitions between the molecular orbitals near the highest occupied molecular orbital (HOMO) and the lowest unoccupied molecular orbital (LUMO) in the metal-Esculetin complex. Charge decomposition analysis (CDA) results demonstrated that these electron transitions originate from the Esculetin fragment to the Zn(II) fragment in the complex. Covalent indexes [(χm)2rc] of the metal ions were found to be correlated with the metal-specific features of the DAS of metal-Esculetin systems. The strength of the linear correlations between the quantitative parameters of the electron density of the bond critical points (BCP) is indicative of the strength of the metal-Esculetin interactions.
Sung-kwon Moon - One of the best experts on this subject based on the ideXlab platform.
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Esculetin Inhibits VEGF-Induced Angiogenesis Both In Vitro and In Vivo.
The American journal of Chinese medicine, 2016Co-Authors: Sung Lyea Park, Wun-jae Kim, Yeon Won, Jun-hui Song, Sook-young Lee, Sung-kwon MoonAbstract:Esculetin is known to inhibit tumor growth, but its effect in angiogenesis has not been studied. Here, we report the efficacy of Esculetin on VEGF-induced angiogenesis. Esculetin treatment inhibited VEGF-induced proliferation and DNA synthesis of HUVECs with no cell toxicity. G1-phase cell-cycle arrest was associated with a decreased expression of cyclins and CDKs via the binding of p27KIP1. Esculetin down-regulated the MMP-2 expression in VEGF-stimulated HUVECs, which suppressed colony tube formation and migration. Esculetin reduced the phosphorylation of VEGFR-2 and the downstream signaling of VEGFR-2, including ERK1/2 and eNOS/Akt pathways. Esculetin suppressed microvessel outgrowth from an aortic ring ex vivo model treated with VEGF, and blocked the VEGF-induced formation of new blood vessels and hemoglobin content in an in vivo Matrigel plug model. Collectively, VEGF-stimulated responses in angiogenesis were inhibited in vitro and in vivo, providing a theoretical basis for effective use against anti-angiogenic therapies.
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p38 MAPK activation is required for Esculetin-induced inhibition of vascular smooth muscle cells proliferation.
Toxicology in vitro : an international journal published in association with BIBRA, 2011Co-Authors: Eun-sun Yun, Sung-suk Park, Wun-jae Kim, Yung Hyun Choi, Ho-chul Shin, Sung-kwon MoonAbstract:The phenolic compound Esculetin is known to inhibit the proliferation of vascular smooth muscle cells (VSMC). However, the signaling pathway by which Esculetin mediates its molecular effects in VSMC remains to be identified. The present results suggest an unexpected role of the p38 MAPK signaling pathway in Esculetin-induced inhibition of VSMC growth. Treatment of VSMC with Esculetin resulted in significant growth inhibition and G1-phase cell-cycle arrest, which was followed by down-regulation of cyclins and cyclin-dependent kinase (CDK) expression. This G1-phase cell-cycle arrest was due to up-regulation of p21WAF1 expression. In addition, Esculetin treatment activated p38 MAPK and ERK1/2. Pretreatment with SB203580, which is a p38 MAPK specific inhibitor, or expression of the dominant negative p38 MAPK (DN p38 MAPK) gene blocked Esculetin-induced p38 MAPK activation and p21WAF1 expression. Finally, both the growth inhibition and the down-regulation of CDKs induced by Esculetin were suppressed by either SB203580 or the DN p38 MAPK mutant gene. In conclusion, these results demonstrate that activation of p38 MAPK contributes to Esculetin-induced p21WAF1 expression in VSMC by decreasing both the cyclin D1/CDK4 and cyclin E/CDK2 complexes. These novel results regarding the molecular mechanism of Esculetin action suggest new preventive and therapeutic treatments for atherosclerosis.
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inhibitory effect of Esculetin on migration invasion and matrix metalloproteinase 9 expression in tnf α induced vascular smooth muscle cells
Molecular Medicine Reports, 2011Co-Authors: Sejung Lee, Wun-jae Kim, Ungsoo Lee, Sung-kwon MoonAbstract:Esculetin, a potent non-competitive inhibitor of lipoxygenase, has been shown to inhibit vascular smooth muscle cell (VSMC) proliferation. However, the effect of Esculetin on the matrix metalloproteinase-9 (MMP-9) regulation responsible for cell migration and invasion has not been previously investigated. The results of the present study showed the Esculetin (12.5-25 µg/ml) induced the inhibition of migration and invasion in tumor necrosis factor-α (TNF-α)-treated VSMC, as demonstrated by a matrigel invasion assay and wound healing analysis. However, Esculetin did not affect cell viability in TNF-α-treated VSMC under 0-25 µg/ml concentration conditions. In addition, both zymographic and immunoblot experiments showed that Esculetin suppressed the TNF-α-induced expression of MMP-9 in VSMC in a dose-dependent manner. Furthermore, the treatment of cells with Esculetin decreased the activity of the TNF-α-induced MMP-9 promoter, which was driven by a luciferase reporter. Finally, Esculetin reduced the binding activities of nuclear factor-κB (NF-κB) and activator protein-1 (AP-1), which are cis-elements present in the promoter of the MMP-9 gene, in TNF-α-treated VSMC. Taken together, these results demonstrated that Esculetin decreased the migration and invasion of cells by suppressing MMP-9 expression, which subsequently reduced the binding activities of NF-κB and AP-1 in TNF-α-treated VSMC. These novel findings provide basic information for effective therapeutic treatment with Esculetin for atherosclerotic disease.
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Esculetin inhibits cell proliferation through the Ras/ERK1/2 pathway in human colon cancer cells.
Oncology reports, 2011Co-Authors: Sung-suk Park, Jung-hyurk Lim, Wun-jae Kim, Sung Kyu Park, Yung Hyun Choi, Sung-kwon MoonAbstract:Esculetin, a phenolic compound, has been shown to inhibit the growth of colon tumors in animal studies. However, the roles of signaling pathways and cell cycle regulation in the Esculetin-induced inhibition of cancer cell growth, remain to be elucidated. The present study suggests a novel mechanism for the Ras/ERK1/2 pathway in Esculetin-treated human colon cancer HCT116 cells. The treatment of cells with Esculetin resulted in significant growth inhibition and G1 phase cell cycle arrest, which led to the down-regulation of cyclin and cyclin-dependent kinase (CDK) expressions. This G1 phase cell cycle arrest was associated with the up-regulation of p27KIP expression. In addition, ERK1/2 was activated by Esculetin. The pre-treatment of cells with the MEK1/2-specific inhibitor, PD98059, blocked the p27KIP expression induced by Esculetin. Blockage of the ERK1/2 function consistently prevented the inhibition of cell proliferation and decreased G1 phase cell cycle protein levels. Furthermore, Ras activation was increased by the Esculetin treatment. Transient transfection of the dominant negative Ras (RasN17) mutant gene abolished both the ERK1/2 activity and p27KIP expression induced by Esculetin. Finally, the overexpression of RasN17 suppressed the Esculetin-induced reduction in cell proliferation and cell cycle proteins. In conclusion, these results indicate that the Ras/ERK1/2 pathway is mediated by the p27KIP1 induction, leading to a reduction in cyclin/CDK complexes in the Esculetin-induced inhibition of colon cancer cell growth. Overall, these findings indicate that the molecular action of Esculetin has therapeutic potential for the treatment of colon malignancies.
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Esculetin inhibits cell proliferation through the ras erk1 2 pathway in human colon cancer cells
Oncology Reports, 2010Co-Authors: Sung-suk Park, Jung-hyurk Lim, Wun-jae Kim, Sung Kyu Park, Yung Hyun Choi, Sung-kwon MoonAbstract:Esculetin, a phenolic compound, has been shown to inhibit the growth of colon tumors in animal studies. However, the roles of signaling pathways and cell cycle regulation in the Esculetin-induced inhibition of cancer cell growth, remain to be elucidated. The present study suggests a novel mechanism for the Ras/ERK1/2 pathway in Esculetin-treated human colon cancer HCT116 cells. The treatment of cells with Esculetin resulted in significant growth inhibition and G1 phase cell cycle arrest, which led to the down-regulation of cyclin and cyclin-dependent kinase (CDK) expressions. This G1 phase cell cycle arrest was associated with the up-regulation of p27KIP expression. In addition, ERK1/2 was activated by Esculetin. The pre-treatment of cells with the MEK1/2-specific inhibitor, PD98059, blocked the p27KIP expression induced by Esculetin. Blockage of the ERK1/2 function consistently prevented the inhibition of cell proliferation and decreased G1 phase cell cycle protein levels. Furthermore, Ras activation was increased by the Esculetin treatment. Transient transfection of the dominant negative Ras (RasN17) mutant gene abolished both the ERK1/2 activity and p27KIP expression induced by Esculetin. Finally, the overexpression of RasN17 suppressed the Esculetin-induced reduction in cell proliferation and cell cycle proteins. In conclusion, these results indicate that the Ras/ERK1/2 pathway is mediated by the p27KIP1 induction, leading to a reduction in cyclin/CDK complexes in the Esculetin-induced inhibition of colon cancer cell growth. Overall, these findings indicate that the molecular action of Esculetin has therapeutic potential for the treatment of colon malignancies.
Chenyang Zhang - One of the best experts on this subject based on the ideXlab platform.
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Interpretation of the differential UV-visible absorbance spectra of metal-NOM complexes based on the quantum chemical simulations for the model compound Esculetin
Chemosphere, 2021Co-Authors: Chenyang Zhang, Xuze Han, Gregory V. Korshin, Andrey M. Kuznetsov, Mingquan YanAbstract:Abstract In this study, the model compound Esculetin that has functional groups typical for natural organic matter (NOM) was used to ascertain the nature of the characteristic bands in the differential UV-visible absorbance spectra (DAS) associated with the formation of metal-NOM complexes. The binding of ten different metal ions (Cu(II), Ni(II), Co(II), Fe(III), Cr(III), Al(III), Zn(II), Ca(II), Mg(II) and Pb(II)) with Esculetin generate four bands in the DAS. These bands are similar to those present in the DAS of metal-NOM complex. The UV-visible absorbance spectra of the metal-Esculetin systems were calculated using time-dependent density functional theory (TD-DFT). The TD-DFT results demonstrate that the prominent features of the DAS of Esculetin are primarily associated with the electron transitions between the molecular orbitals near the highest occupied molecular orbital (HOMO) and the lowest unoccupied molecular orbital (LUMO) in the metal-Esculetin complex. Charge decomposition analysis (CDA) results demonstrated that these electron transitions originate from the Esculetin fragment to the Zn(II) fragment in the complex. Covalent indexes [(χm)2rc] of the metal ions were found to be correlated with the metal-specific features of the DAS of metal-Esculetin systems. The strength of the linear correlations between the quantitative parameters of the electron density of the bond critical points (BCP) is indicative of the strength of the metal-Esculetin interactions.
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interpretation of the differential uv visible absorbance spectra of metal nom complexes based on the quantum chemical simulations for the model compound Esculetin
Chemosphere, 2021Co-Authors: Chenyang Zhang, Xuze Han, Gregory V. Korshin, Andrey M. Kuznetsov, Mingquan YanAbstract:In this study, the model compound Esculetin that has functional groups typical for natural organic matter (NOM) was used to ascertain the nature of the characteristic bands in the differential UV-visible absorbance spectra (DAS) associated with the formation of metal-NOM complexes. The binding of ten different metal ions (Cu(II), Ni(II), Co(II), Fe(III), Cr(III), Al(III), Zn(II), Ca(II), Mg(II) and Pb(II)) with Esculetin generate four bands in the DAS. These bands are similar to those present in the DAS of metal-NOM complexes. The UV-visible absorbance spectra of the metal-Esculetin systems were calculated using time-dependent density functional theory (TD-DFT). The TD-DFT results demonstrate that the prominent features of the DAS of Esculetin are primarily associated with the electron transitions between the molecular orbitals near the highest occupied molecular orbital (HOMO) and the lowest unoccupied molecular orbital (LUMO) in the metal-Esculetin complex. Charge decomposition analysis (CDA) results demonstrated that these electron transitions originate from the Esculetin fragment to the Zn(II) fragment in the complex. Covalent indexes [(χm)2rc] of the metal ions were found to be correlated with the metal-specific features of the DAS of metal-Esculetin systems. The strength of the linear correlations between the quantitative parameters of the electron density of the bond critical points (BCP) is indicative of the strength of the metal-Esculetin interactions.
Yung Hyun Choi - One of the best experts on this subject based on the ideXlab platform.
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Esculetin induces apoptosis through egfr pi3k akt signaling pathway and nucleophosmin relocalization
Journal of Cellular Biochemistry, 2016Co-Authors: Young Joo Jeon, Yung Hyun Choi, Junghyun Shim, Jin Hyoung Cho, Seung-yeop Lee, Hong-ju Park, Seunggon Jung, Jung Il ChaeAbstract:Esculetin, a coumarin compound, has anti-proliferative effects on various types of human cancer cells, but its effect on oral squamous cell carcinoma (OSCC) is unknown. In this study, we determined whether Esculetin had anti-proliferative effects on two oral squamous cell lines, HN22, and HSC2. We found that Esculetin inhibited cell viability by inducing apoptosis, as evinced by apoptotic cell morphologies, nuclear fragmentation, and the multi-caspase/MMP activity. Furthermore, proteomic analysis was used to identify the target-specific proteins involved in Esculetin treatment. Intriguingly, apoptotic cell death by Esculetin was associated with significant inhibition of the EGFR/PI3K/Akt signaling pathway. We also demonstrated that the expression of nucleophosmin (NPM) markedly decreased after Esculetin treatment, and relocalization of NPM from the nucleous to the cytoplasm, together with p65, potentiated apoptotic stimulation. Additionally, our data indicated that NPM expression was markedly higher in OSCC tissues than in normal tissues. Our results collectively indicated that Esculetin inhibited the proliferation of OSCC through EGFR-mediated signaling pathways and down-regulation of NPM as well as the perturbation of NPM trafficking from the nucleolus to the cytoplasm resulted in apoptosis.
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Esculetin Induces Apoptosis through EGFR/PI3K/Akt Signaling Pathway and Nucleophosmin Relocalization.
Journal of cellular biochemistry, 2015Co-Authors: Young Joo Jeon, Yung Hyun Choi, Junghyun Shim, Jin Hyoung Cho, Seung-yeop Lee, Hong-ju Park, Seunggon Jung, Jung Il ChaeAbstract:Esculetin, a coumarin compound, has anti-proliferative effects on various types of human cancer cells, but its effect on oral squamous cell carcinoma (OSCC) is unknown. In this study, we determined whether Esculetin had anti-proliferative effects on two oral squamous cell lines, HN22, and HSC2. We found that Esculetin inhibited cell viability by inducing apoptosis, as evinced by apoptotic cell morphologies, nuclear fragmentation, and the multi-caspase/MMP activity. Furthermore, proteomic analysis was used to identify the target-specific proteins involved in Esculetin treatment. Intriguingly, apoptotic cell death by Esculetin was associated with significant inhibition of the EGFR/PI3K/Akt signaling pathway. We also demonstrated that the expression of nucleophosmin (NPM) markedly decreased after Esculetin treatment, and relocalization of NPM from the nucleous to the cytoplasm, together with p65, potentiated apoptotic stimulation. Additionally, our data indicated that NPM expression was markedly higher in OSCC tissues than in normal tissues. Our results collectively indicated that Esculetin inhibited the proliferation of OSCC through EGFR-mediated signaling pathways and down-regulation of NPM as well as the perturbation of NPM trafficking from the nucleolus to the cytoplasm resulted in apoptosis.
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Esculetin 6 7 dihydroxycoumarin a potential cancer chemopreventive agent through suppression of sp1 in oral squamous cancer cells
International Journal of Oncology, 2015Co-Authors: Jin Hyoung Cho, Yung Hyun Choi, Junghyun Shim, Jaecheon Shin, Jungjae Cho, Jung Il ChaeAbstract:Esculetin (6,7-dihydroxycoumarin), a coumarin compound, is known to inhibit proliferation and induce apoptosis in several types of human cancer cells and is regarded as a promising chemotherapeutic agent. The purpose of the present study was to investigate the anti-proliferative effects of Esculetin on two oral squamous cell carcinoma (OSCC) cell lines, HN22 and HSC4, through regulation of specificity protein 1 (Sp1). We examined the apoptotic effects of Esculetin were measured by MTS assay, DAPI staining, Annexin V, PI staining, RT-PCR, western blot analysis and immunocytochemistry in HN22 and HSC4 cells. Taken together, the results of the present study indicate that Esculetin had anti-proliferative effect on the growth of OSCC cells (HN22 and HSC4) in a dose- and time-dependent manner. The treatment of HN22 and HSC4 cells with Esculetin led to a significant reduction in growth and induced apoptosis, followed by the regulation of Sp1 and Sp1 regulatory protein. This indicates that Esculetin inhibited cell growth and induced apoptosis by suppressing Sp1 in HN22 and HSC4 cells, suggesting it to be a potent anticancer drug candidate for oral cancer.
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Esculetin suppresses lipopolysaccharide induced inflammatory mediators and cytokines by inhibiting nuclear factor κb translocation in raw 264 7 macrophages
Molecular Medicine Reports, 2014Co-Authors: Su Hyun Hong, Cheol Park, Min Ho Han, Huikyung Jeong, Yung Hyun ChoiAbstract:Although previous studies have demonstrated that the natural coumarin compound Esculetin possesses various pharmacological properties, the molecular mechanism of Esculetin-mediated anti-inflammatory potential is not fully understood. In this study, we determined the effects of Esculetin on lipopolysaccharide (LPS)-induced inflammatory responses of murine RAW 264.7 macrophages. The results indicate that Esculetin inhibits LPS-induced nitric oxide and prostaglandin E2 production in a concentration-dependent manner, and inhibits inducible nitric oxide synthase and cyclooxygenase-2 expression in RAW 264.7 cells. Esculetin also significantly suppresses the production of inflammatory cytokines, including tumor necrosis factor-α and interleukin-1β, which was concomitant with a decrease in their expression levels. Furthermore, it was observed that Esculetin attenuated the LPS-mediated nuclear factor-kappa B (NF-κB) translocation associated with the blocking of inhibitor of NF-κB (IκB)-α degradation as well as reactive oxygen species (ROS) production, without any significant cytotoxicity. These data suggest that, by blocking NF-κB activation, Esculetin suppresses LPS-elicited inflammatory events, and this is mediated, at least in part, by inhibiting the generation of ROS. Collectively, these findings provide mechanistic insights into the anti-inflammatory action of Esculetin in macrophages.
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p38 MAPK activation is required for Esculetin-induced inhibition of vascular smooth muscle cells proliferation.
Toxicology in vitro : an international journal published in association with BIBRA, 2011Co-Authors: Eun-sun Yun, Sung-suk Park, Wun-jae Kim, Yung Hyun Choi, Ho-chul Shin, Sung-kwon MoonAbstract:The phenolic compound Esculetin is known to inhibit the proliferation of vascular smooth muscle cells (VSMC). However, the signaling pathway by which Esculetin mediates its molecular effects in VSMC remains to be identified. The present results suggest an unexpected role of the p38 MAPK signaling pathway in Esculetin-induced inhibition of VSMC growth. Treatment of VSMC with Esculetin resulted in significant growth inhibition and G1-phase cell-cycle arrest, which was followed by down-regulation of cyclins and cyclin-dependent kinase (CDK) expression. This G1-phase cell-cycle arrest was due to up-regulation of p21WAF1 expression. In addition, Esculetin treatment activated p38 MAPK and ERK1/2. Pretreatment with SB203580, which is a p38 MAPK specific inhibitor, or expression of the dominant negative p38 MAPK (DN p38 MAPK) gene blocked Esculetin-induced p38 MAPK activation and p21WAF1 expression. Finally, both the growth inhibition and the down-regulation of CDKs induced by Esculetin were suppressed by either SB203580 or the DN p38 MAPK mutant gene. In conclusion, these results demonstrate that activation of p38 MAPK contributes to Esculetin-induced p21WAF1 expression in VSMC by decreasing both the cyclin D1/CDK4 and cyclin E/CDK2 complexes. These novel results regarding the molecular mechanism of Esculetin action suggest new preventive and therapeutic treatments for atherosclerosis.
Andrey M. Kuznetsov - One of the best experts on this subject based on the ideXlab platform.
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Interpretation of the differential UV-visible absorbance spectra of metal-NOM complexes based on the quantum chemical simulations for the model compound Esculetin
Chemosphere, 2021Co-Authors: Chenyang Zhang, Xuze Han, Gregory V. Korshin, Andrey M. Kuznetsov, Mingquan YanAbstract:Abstract In this study, the model compound Esculetin that has functional groups typical for natural organic matter (NOM) was used to ascertain the nature of the characteristic bands in the differential UV-visible absorbance spectra (DAS) associated with the formation of metal-NOM complexes. The binding of ten different metal ions (Cu(II), Ni(II), Co(II), Fe(III), Cr(III), Al(III), Zn(II), Ca(II), Mg(II) and Pb(II)) with Esculetin generate four bands in the DAS. These bands are similar to those present in the DAS of metal-NOM complex. The UV-visible absorbance spectra of the metal-Esculetin systems were calculated using time-dependent density functional theory (TD-DFT). The TD-DFT results demonstrate that the prominent features of the DAS of Esculetin are primarily associated with the electron transitions between the molecular orbitals near the highest occupied molecular orbital (HOMO) and the lowest unoccupied molecular orbital (LUMO) in the metal-Esculetin complex. Charge decomposition analysis (CDA) results demonstrated that these electron transitions originate from the Esculetin fragment to the Zn(II) fragment in the complex. Covalent indexes [(χm)2rc] of the metal ions were found to be correlated with the metal-specific features of the DAS of metal-Esculetin systems. The strength of the linear correlations between the quantitative parameters of the electron density of the bond critical points (BCP) is indicative of the strength of the metal-Esculetin interactions.
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interpretation of the differential uv visible absorbance spectra of metal nom complexes based on the quantum chemical simulations for the model compound Esculetin
Chemosphere, 2021Co-Authors: Chenyang Zhang, Xuze Han, Gregory V. Korshin, Andrey M. Kuznetsov, Mingquan YanAbstract:In this study, the model compound Esculetin that has functional groups typical for natural organic matter (NOM) was used to ascertain the nature of the characteristic bands in the differential UV-visible absorbance spectra (DAS) associated with the formation of metal-NOM complexes. The binding of ten different metal ions (Cu(II), Ni(II), Co(II), Fe(III), Cr(III), Al(III), Zn(II), Ca(II), Mg(II) and Pb(II)) with Esculetin generate four bands in the DAS. These bands are similar to those present in the DAS of metal-NOM complexes. The UV-visible absorbance spectra of the metal-Esculetin systems were calculated using time-dependent density functional theory (TD-DFT). The TD-DFT results demonstrate that the prominent features of the DAS of Esculetin are primarily associated with the electron transitions between the molecular orbitals near the highest occupied molecular orbital (HOMO) and the lowest unoccupied molecular orbital (LUMO) in the metal-Esculetin complex. Charge decomposition analysis (CDA) results demonstrated that these electron transitions originate from the Esculetin fragment to the Zn(II) fragment in the complex. Covalent indexes [(χm)2rc] of the metal ions were found to be correlated with the metal-specific features of the DAS of metal-Esculetin systems. The strength of the linear correlations between the quantitative parameters of the electron density of the bond critical points (BCP) is indicative of the strength of the metal-Esculetin interactions.