Four new bivalent nickel hydrazone complexes have been synthesised from the reactions of [NiCl2(PPh3)2] with H2L {L = dianion of the hydrazones derived from the condensation of salicylaldehyde or o-hydroxy acetophenone with p-toluic acid hydrazide (H2L1) (1), (H2L2) (2) and o-hydroxy acetophenone or o-hydroxy naphthaldehyde with benzhydrazide (H2L3) (3) and (H2L4) (4)} and formulated as [Ni(L1)(PPh3)] (5), [Ni(L2)(PPh3)] (6), [Ni(L3)(PPh3)] (7) and [Ni(L4)(PPh3)] (8). Structural characterization of complexes 5–8 were accomplished by using various physico-chemical techniques. In order to study the influence of substitution in the ligand and its planarity on the biological activity of complexes 5–8 containing them, suitable hydrazone ligands 1–4 have been selected in this study. Single crystal diffraction data of complexes 5, 7 and 8 proved the geometry of the complexes to be distorted square planar with a 1:1 ratio between the metal ion and the coordinated hydrazones. To provide more insight on the mode of action of complexes 5–8 under biological conditions, additional experiments involving their interaction with calf thymus DNA (CT DNA) and bovine serum albumin (BSA) were monitored by UV-visible and fluorescence titrations respectively. Further, the ligands 1–4 and corresponding nickel(II) chelates 5–8 have been tested for their scavenging effect towards OH and O2− radicals. The effect of complexes 5–8 to arrest the growth of HeLa and Hep-2 tumour cell lines has been studied along with the cell viability against the non-cancerous NIH 3T3 cells under in vitro conditions.

Four new bivalent nickel hydrazone complexes have been synthesised from the reactions of [NiCl2(PPh3)2] with H2L {L = dianion of the hydrazones derived from the condensation of salicylaldehyde or o-hydroxy acetophenone with p-toluic acid hydrazide (H2L1) (1), (H2L2) (2) and o-hydroxy acetophenone or o-hydroxy naphthaldehyde with benzhydrazide (H2L3) (3) and (H2L4) (4)} and formulated as [Ni(L1)(PPh3)] (5), [Ni(L2)(PPh3)] (6), [Ni(L3)(PPh3)] (7) and [Ni(L4)(PPh3)] (8). Structural characterization of complexes 5–8 were accomplished by using various physico-chemical techniques. In order to study the influence of substitution in the ligand and its planarity on the biological activity of complexes 5–8 containing them, suitable hydrazone ligands 1–4 have been selected in this study. Single crystal diffraction data of complexes 5, 7 and 8 proved the geometry of the complexes to be distorted square planar with a 1:1 ratio between the metal ion and the coordinated hydrazones. To provide more insight on the mode of action of complexes 5–8 under biological conditions, additional experiments involving their interaction with calf thymus DNA (CT DNA) and bovine serum albumin (BSA) were monitored by UV-visible and fluorescence titrations respectively. Further, the ligands 1–4 and corresponding nickel(II) chelates 5–8 have been tested for their scavenging effect towards OH and O2− radicals. The effect of complexes 5–8 to arrest the growth of HeLa and Hep-2 tumour cell lines has been studied along with the cell viability against the non-cancerous NIH 3T3 cells under in vitro conditions.

A set each of new bivalent and trivalent ruthenium complexes, [RuIII(HL)Cl2(EPh3)2] and [RuII(L)(CO)(EPh3)2] (E = P (complexes 1 and 2) or As (complexes 3 and 4)) were synthesised from the reactions of [RuIIICl3(EPh3)3] with 2-hydroxynaphthaldehyde benzoic acid hydrazone (H2L) in methanol–chloroform and characterized by elemental analysis, spectral data and XRD study. A suitable mechanism to account for the formation of bivalent ruthenium carbonyl complexes from the corresponding trivalent precursors is provided by considering the role of added base in the reaction. Interaction of complexes 1–4 with CT-DNA/bovine serum albumin was analysed with absorption and emission spectral titration studies. In vitro cytotoxic potential of the above ruthenium hydrazone complexes 1–4 assayed against the A549 cell line revealed a significant growth inhibition. The test complexes 1–4 added in IC50 concentration into the cell culture medium enhanced the release of lactate dehydrogenase, NO and reactive oxygen species in comparison with the control. Cell death induced by the complexes was studied using a propidium iodide staining assay and showed noticeable changes in the cell morphology which resembled apoptosis.

A set each of new bivalent and trivalent ruthenium complexes, [RuIII(HL)Cl2(EPh3)2] and [RuII(L)(CO)(EPh3)2] (E = P (complexes 1 and 2) or As (complexes 3 and 4)) were synthesised from the reactions of [RuIIICl3(EPh3)3] with 2-hydroxynaphthaldehyde benzoic acid hydrazone (H2L) in methanol–chloroform and characterized by elemental analysis, spectral data and XRD study. A suitable mechanism to account for the formation of bivalent ruthenium carbonyl complexes from the corresponding trivalent precursors is provided by considering the role of added base in the reaction. Interaction of complexes 1–4 with CT-DNA/bovine serum albumin was analysed with absorption and emission spectral titration studies. In vitro cytotoxic potential of the above ruthenium hydrazone complexes 1–4 assayed against the A549 cell line revealed a significant growth inhibition. The test complexes 1–4 added in IC50 concentration into the cell culture medium enhanced the release of lactate dehydrogenase, NO and reactive oxygen species in comparison with the control. Cell death induced by the complexes was studied using a propidium iodide staining assay and showed noticeable changes in the cell morphology which resembled apoptosis.