Iron(III) bis‐complexes of Schiff bases of <i>S</i>‐methyldithiocarbazates: Synthesis, structure, spectral and redox properties and cytotoxicity

Abstract

A series of iron(III) bis‐complexes of the type [FeL 2 ]X 1‐4 , X = OH − ( 1 ), Cl ¯ ( 3 ), and FeCl 4 ¯ ( 2 , 4 ), where LH is a tridentate (N,N,S) ligands such as N ′‐(1‐pyridin‐2‐ylethylidene)‐hydrazinecarbodithioic acid methyl ester ( HL1 ), N ′‐(phenylpyridin‐2‐ylmethylene)‐hydrazinecarbodithioic acid methyl ester ( HL2 ), N ′‐quinolin‐2‐ylmethylene‐hydrazinecarbodithioic acid methyl ester ( HL3 ), or N ′‐(1‐methyl‐1 H ‐imidazol‐2‐yl‐methylene)hydrazinecarbodithioic acid methyl ester ( HL4 ) has been isolated in moderate to good yields and completely characterized by elemental analyses, conductivity studies, and infrared and UV‐visible spectral measurements. The single crystal X‐ray structures of 1 , 2 and 4 revealed that two deprotonated tridentate (NNS) ligands are meridionally coordinated to constitute a distorted octahedral coordination geometry around iron(III). In acetonitrile solution, all the complexes show quasi‐reversible Fe(III)/Fe(II) redox behavior. The in vitro cytotoxicity of the ligands HL1–HL4 (IC 50 : HL1 , 64.5; HL2 , 51.0; HL3 , 124.0; HL4 , 45.0 μM at 24 h) and complexes 1–4 (IC 50 : 1 , 84.5; 2 , 40.0; 3 , 168.5; 4 , 50.5 μM at 24 h) towards A549 lung cancer cell lines are similar to cisplatin (69.0 μM), revealing that free ligands cause cancer cell death with potency higher than the corresponding iron(III) complexes. Also, both the ligands and the complexes cause cell death mainly through apoptotic mode, as revealed by the observation of a higher percentage of apoptotic cells in acridine orange (AO)/ ethidium bromide (EB), and Annexin V‐Cy3 stained cancer cells.