Synthesis, characterization and in vitro biological activities of new water-soluble copper(II), zinc(II), and nickel(II) complexes with sulfonato-substituted Schiff base ligand

Abstract

A water-soluble thiosemicarbazone Schiff base ligand, namely sodium 3-{[(aminocarbonothioyl)hydrazono]methyl}-4-hydroxybenzenesulfonate (NaH2L) was prepared by 1:1 condensation of sodium salicylaldehyde-5-sulfonate and thiosemicarbazide. The X-ray structure analysis of NaH2L shows that the organic fragments of the ligand are bridged by two different types of seven-coordinated sodium cations. The ligand was used in the synthesis of the following CuII, NiII, and ZnII complexes: [Cu2(HL)2(H2O)3] (1), Ni(HL)(H2O)1.5 (2), and Zn(HL)(H2O)2 (3). The metal complexes were characterized by physico-chemical and spectroscopic methods. The X-ray structure analysis of the dinuclear copper complex (1) shows that two metal centers are five coordinated having distorted square pyramidal geometries. There are significant π-π interactions between the phenyl rings of the two ligands in the complex with the centroid-centroid distance 3.8571(10)Å. Solubility in water at 25°C was measured 100g/L for NaH2L, 50g/L for 1, 100g/L for 2 and 0.1g/L for 3. The stability of NaH2L, 1 and 2 in water solution exceeded 4days. The compounds 1 and 2 showed low antimicrobial activity while the inhibition efficiency of NaH2L and 3 was negligible. The ligand and complexes were evaluated for scavenging activity of picrylhydrazyl radical (DPPH) and ferric reducing antioxidant power (FRAP), using l-ascorbic acid (Vitamin C) as a reference antioxidant. The strongest radical scavenging was found for NaH2L. Cytotoxicity of the compounds was investigated against the human chronic myeloid leukemia K562 cells by the MTT assay method. The strongest cytotoxicity was found for 1 with the IC50 value of 16±1.0μg/mL for 72h and therefore 1 was chosen for further studies. The compound 1 caused a noticeable decrease in viability of the K562 cells in a dose- and time-dependent manner and induced apoptosis in the K562 cell line.