期刊
DALTON TRANSACTIONS
卷 50, 期 38, 页码 13374-13386出版社
ROYAL SOC CHEMISTRY
DOI: 10.1039/d1dt01740c
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A new end-off compartmental Mannich ligand HL1 was synthesized and found to form a Cu(II) complex with Cu(ClO4)2, while a new Cu(II) complex HLF was formed through chemical reactions. The two complexes exhibited different anticancer activities on lung adenocarcinoma cells (A549), with complex 1 showing stronger inhibition of cell proliferation and induction of apoptosis in A549 cells.
A new end-off compartmental Mannich ligand (HL1) namely 3-((bis(2-methoxyethyl)amino)methyl)-5-bromo-2-hydroxybenzaldehyde containing two methoxyethyl pendant arms and one-CHO functionality has been synthesized through conventional C-C and C N coupling reactions. On treatment with Cu (ClO4)(2), HL1 yields a dinuclear mu-phenolatocopper(II) complex having the molecular formula [Cu-2(L-1)(2)] (ClO4)(2)(H2O)(1.5) (1). Surprisingly, the ligand HL1 is radically transformed into a new asymmetric Schiff-Mannich base ligand (HLF) in the presence of NaN3 and Cu(ClO4)(2) forming a unique dinuclear centrosymmetric Cu(II) complex [Cu(L-F)](2) (2) as evident from single-crystal X-ray diffraction (SCXRD) analysis. A probable mechanistic rationalization has been proposed on the basis of theoretical calculations, which suggests systematic fragmentation of HL1 in the presence of azide residue and re-condensation of the fragmented units to yield the final Cu-HLF complex (2). SCXRD analysis portrays a large inter-metallic distance in complex 2 in comparison with complex 1 (5.493 vs. 2.989 angstrom, respectively) along with other distinct structural features. After physicochemical characterization both the complexes have been exploited to evaluate their possible anticancer proficiency on lung adenocarcinoma cell line (A549). Complex 1 distinctly impeded the proliferation of lung adenocarcinoma cells in a dose-dependent manner more efficiently than complex 2. Due to the behavior of complex 1 as potential therapeutics, cellular transformations of A549 cells have been systematically investigated. As evidenced from various in vitro experiments, the cell death mechanism triggered by complex 1 turned out to be apoptosis, as indicated by the DNA fragmentation, chromatin condensation, membrane blebbing and imbalanced cell cycle distribution as well as retard migration in A549 cells.
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