A series of mixed ligand ruthenium(II) complexes [Ru(Hdpa)₂(diimine)](ClO₄)₂1–5, where Hdpa is 2,2′-dipyridylamine and diimine is 1,10-phenanthroline (phen) and a modified/extended 1,10-phenanthroline such as, 5,6-dimethyl-1,10-phenanthroline (5,6-dmp), dipyrido[3,2-d:2′,3′-f]quinoxaline (dpq), 5-methyldipyrido[3,2-d:2′,3′-f]quinoxaline (mdpq) and dipyrido[3,2-a:2′,3′-c]phenazine (dppz) have been isolated and characterized by analytical and spectral methods. The complex [Ru(Hdpa)₂(phen)](PF₆)₂1 has been structurally characterized and the coordination geometry around Ru(II) in it is described as distorted octahedral. ¹H NMR spectral data reveal that 1–5 should have a C₂ symmetry lying on the diimine plane due to the rapid flapping of the coordinated Hdpa ligands. The interaction of the complexes with calf thymus (CT) DNA has been explored by using absorption and emission spectral and viscometry and electrochemical techniques and the mode of DNA binding of the complexes has been proposed. The DNA binding affinity of the complexes decreases with decrease in number of planar aromatic rings in the co-ligand supporting the intercalation of the diimine co-ligands in between the DNA base pairs. Circular dichroic spectral studies reveal that the complexes 3–5 exhibit induced circular dichroism upon binding to CT DNA. Interestingly, upon interaction with CT DNA all the complexes show an increase in anodic current in the cyclic voltammograms suggesting that they are involved in electrocatalytic guanine oxidation. Interestingly, of all the complexes, only 5 alters the DNA superhelicity upon binding with supercoiled pBR322 DNA, which is consistent with its higher DNA binding affinity. Further, the cytotoxicities of the complexes against human cervical epidermoid carcinoma cell line (ME180) have been examined. Interestingly, 5 exhibits a cytotoxicity against ME180 higher than other complexes with potency approximately 8 times more than cisplatin for 24 h incubation but 4 times lower than cisplatin for 48 h incubation.

A series of mixed ligand ruthenium(II) complexes [Ru(pdto)(diimine)](ClO₄)₂/(PF₆)₂1–3 and [Ru(bbdo)(diimine)](ClO₄)₂4–6, where pdto is 1,8-bis(pyrid-2-yl)-3,6-dithiooctane, bbdo is 1,8-bis(benzimidazol-2-yl)-3,6-dithiooctane and diimine is 1,10-phenanthroline (phen), dipyrido-[3,2-d:2′,3′-f]-quinoxaline (dpq) and dipyrido[3,2-a:2′,3′-c]phenazine (dppz), have been isolated and characterised by analytical and spectral methods. The complexes [Ru(pdto)(phen)](PF₆)₂1a, [Ru(pdto)(dpq)(Cl)](PF₆) 2a, [Ru(bbdo)(phen)](PF₆)₂4a and [Ru(bbdo)(dpq)](ClO₄)₂5 have been structurally characterized and their coordination geometries around ruthenium(II) are described as distorted octahedral. In 1a, 4a and 5 the two thioether sulfur and two py/bzim nitrogen atoms of the tetradentate pdto/bbdo ligand are folded around Ru(II) to give predominantly a “cis-α” configuration. ^IH NMR spectral data of the complexes support this configuration in solution. In [Ru(pdto)(dpq)Cl](PF₆) 2a with a distorted octahedral coordination geometry, one of the two py nitrogens of pdto is not coordinated. The DNA binding constants (K_b : 2, 2.00 ± 0.02 × 10⁴ M⁻¹, s = 1.0; 3, 3.00 ± 0.01 × 10⁶ M⁻¹, s = 1.3) determined by absorption spectral titrations of the complexes with CT DNA reveal that 3 interacts with DNA more tightly than 2 through partial intercalation of the extended planar ring of coordinated dppz with the DNA base stack. The DNA binding affinities of the complexes increase with increase in the number of planar aromatic rings in the co-ligand, and on replacing both the py moieties in pdto complexes (1–3) by bzim moieties to give bbdo complexes (4–6). Upon interaction with CT DNA the complexes 1, 2, 5 and 6 show a decrease in anodic current in the cyclic voltammograms. On the other hand, interestingly, 3 and 4 show an increase in anodic current suggesting their involvement in electrocatalytic guanine oxidation. Interestingly, of all the complexes, only 6 alters the superhelicity of DNA upon binding with supercoiled pBR322 DNA. The cytotoxicities of the dppz complexes 3 and 6, which avidly bind to DNA, have been examined by screening them against cell lines of different cancer origins. It is noteworthy that 6 exhibits selectivity with higher cytotoxicity against the melanoma cancer cell line (A375) than other cell lines, potency approximately twice that of cisplatin and toxicity to normal cells 3 and 90 times less than cisplatin and adriamycin respectively.

A series of water soluble copper(II) complexes of the types [Cu(L)Cl] 1–2, where LH is 2-(2-(1H-benzimidazol-2-yl)ethyliminomethyl)phenol (H(L1)), and 2-(2-(1H-benzimidazol-2-yl)-ethyliminomethyl)-4-methylphenol (H(L2)), and [Cu(L)Cl₂] 3–6, where L is (2-pyridin-2-yl-ethyl)pyridin-2-ylmethyleneamine (L3), 2-(1H-benzimidazol-2-yl)ethylpyridin-2-yl-methyleneamine (L4), 2-(1H-benzimidazol-2-yl)ethyl(1H-imidazol-2-ylmethylene)amine (L5), and 2-(1H-benzimidazol-2-yl)ethyl-(4,4a-dihydroquinolin-2-ylmethylene)amine (L6), have been isolated and characterized by elemental analysis, electronic absorption, ESI-MS and EPR spectral techniques and the electrochemical method. The single crystal X-ray structures of [Cu(L1)Cl] 1 and [Cu(L2)Cl] 2 possess a distorted square-based coordination geometry while [Cu(L4)Cl₂] 4 and [Cu(L6)Cl₂] 6 possess a distorted trigonal bipyramidal coordination geometry. Both absorption spectral titration and an EthBr displacement assay reveal that all the complexes bind with calf thymus (CT) DNA through covalent mode of DNA interaction involving the replacement of an easily removable chloride ion with DNA nucleobases. All the complexes exhibit oxidative cleavage of supercoiled (SC) plasmid DNA in the presence of hydrogen peroxide as an activator. It is remarkable that at 50 μM concentration 5 and 6 completely degrade SC DNA into undetectable minor fragments and thus they act as efficient chemical nucleases. All the complexes are remarkable in displaying cytotoxicity against the HBL-100 human breast cancer cell line with potency more than that of the widely used drug cisplatin and hence they have the potential to act as promising anticancer drugs. Interestingly, they are non-toxic to normal cell lymphocytes isolated from human blood samples, revealing that they are selective in killing only the cancer cells.

Several mononuclear Ni(II) complexes of the type [Ni(L)(CH₃CN)₂](BPh₄)₂1–7, where L is a tetradentate tripodal 4N ligand such as N,N-dimethyl-N′,N′-bis(pyrid-2-ylmethyl)ethane-1,2-diamine (L1), N,N-diethyl-N′,N′-bis(pyrid-2-ylmethyl)ethane-1,2-diamine (L2), N,N-dimethyl-N′-(1-methyl-1H-imidazol-2-ylmethyl)-N′-(pyrid-2-ylmethyl)ethane-1,2-diamine (L3), N,N-dimethyl-N′,N′-bis(1-methyl-1H-imidazol-2-ylmethyl)ethane-1,2-diamine (L4), N,N-dimethyl-N′,N′-bis(quinolin-2-ylmethyl)ethane-1,2-diamine (L5), tris(benzimidazol-2-ylmethyl)amine (L6) and tris(pyrid-2-ylmethyl)amine (L7), have been isolated and characterized using CHN analysis, UV-Visible spectroscopy and mass spectrometry. The single-crystal X-ray structures of the complexes [Ni(L1)(CH₃CN)(H₂O)](ClO₄)₂1a, [Ni(L2)(CH₃CN)₂](BPh₄)₂2, [Ni(L3)(CH₃CN)₂](BPh₄)₂3 and [Ni(L4)(CH₃CN)₂](BPh₄)₂4 have been determined. All these complexes possess a distorted octahedral coordination geometry in which Ni(II) is coordinated to four nitrogen atoms of the tetradentate ligands and two CH₃CN (2, 3, 4) or one H₂O and one CH₃CN (1a) are located in cis positions. The Ni–N_py bond distances (2.054(2)–2.078(3) Å) in 1a, 2 and 3 are shorter than the Ni–N_amine bonds (2.127(2)–2.196(3) Å) because of sp² and sp³ hybridizations of the pyridyl and tertiary amine nitrogens respectively. In 3 the Ni–N_im bond (2.040(5) Å) is shorter than the Ni–N_py bond (2.074(4) Å) due to the stronger coordination of imidazole compared with the pyridine donor. In dichloromethane/acetonitrile solvent mixture, all the Ni(II) complexes possess an octahedral coordination geometry, as revealed by the characteristic ligand field bands in the visible region. They efficiently catalyze the hydroxylation of alkanes when m-CPBA is used as oxidant with turnover number (TON) in the range of 340–620 and good alcohol selectivity for cyclohexane (A/K, 5–9). By replacing one of the pyridyl donors in TPA by a weakly coordinating –NMe₂ or –NEt₂ donor nitrogen atom the catalytic activity decreases slightly with no change in the selectivity. In contrast, upon replacing the pyridyl nitrogen donor by the strongly σ-bonding imidazolyl or sterically demanding quinolyl/benzimidazolyl nitrogen donor, both the catalytic activity and selectivity decrease, possibly due to destabilization of the intermediate [(4N)(CH₃CN)Ni–O˙]⁺ radical species. Adamantane is selectively (3°/2°, 12–17) oxidized to 1-adamantanol, 2-adamantanol and 2-adamantanone while cumene is selectively oxidized to 2-phenyl-2-propanol. In contrast to cyclohexane oxidation, the incorporation of sterically hindering quinolyl/benzimidazolyl donors around Ni(II) leads to a high 3°/2° bond selectivity for adamantane oxidation. A linear correlation between the metal–ligand covalency parameter (β) and the turnover number has been observed.