Supramolecular assemblies of new pseudohalide end-to-end bridged copper(II) complex and molecular structural variety of penta and hexa-coordinted metal(II) complexes with hydrazido-based ligand

Abstract

With an hydrazido-based ligand, C14H13N2O and Cu, Ni metal(II) salts, three new mononuclear [Ni(HL)(NO3)(H2O)]NO3,C14H15N5NiO8, 1, [Cu(HL)(H2O)2]2NO3, C14H17CuN5O4, 2, [Ni(HL)2]2ClO4, C28H30Cl2N6NiO12, 3 and one binuclear end-to-end thiocynate bridged [Cu2(μ-SCN)2(L)2], C30H24Cu2N8O2S2, 4 complexes have been synthesized and characterized by physico-chemical techniques. All of the complexes were structurally characterized using single crystal X-ray diffraction. Complexes 1 and 2 have a penta-coordinated environment around the metal(II) centre, whereas complex 3 has a distorted hexa-coordinated geometry. In complex 4 two symmetry related, adjacent copper(II) coordination moieties are joined end-to-end in an unprecedented manner forming a thiocynate bridged, yielding a dicopper entity. The presence of two “symmetric” thiocynate bridges with Cu-SCN and Cu-NCS distances of 2.832 Å and 1.925 Å, respectively, results in a Cu⋯Cu distance of 5.503 Å. Binuclear complex, 4 exhibits a weak antiferromagnetic interaction between adjacent copper(II) centres. These copper(II) mononuclear and binuclear complexes have also been studied by X-band EPR spectroscopy. The crystal packing of these new complexes is stabilized by H-bonding, weak intermolecular interactions, CH⋯π and π⋯π interactions. Electrochemical data (CV and DPV) for the complexes shows MII → MI reduction activity. Electronic spectroscopy and computational features are examined by quantum chemical studies. The inhibitory effect of the complexes were tested on a cell population with IMR 32 (neuroblastoma), MCF 7 (breast cancer), HepG2 (hepatocellular carcinoma), L132 (lung cells) cell lines by MTT assay. Complex 3 showed a prominent cytotoxicity against the all cell lines. Expression levels of the Bax (pro-apoptotic) and Bcl2 (anti-apoptotic) genes were also studied, wherein the genes of interest showed a moderate down regulation after treatment with complexes 1 and 3. Finally, antioxidant superoxide dismutase activity measurements show that the complexes behave as superoxide dismutase mimics.