Metal complexes with organelle specificity and potent but selective cytotoxicity are highly desirable. In this work, we report the synthesis, characterization and cytotoxicity of six novel copper(II) complexes of the formula [Cu(R-tpy)(N-O)]NO₃ (1–6), where R-tpy is 4′-phenyl-2,2′:6′,2′′-terpyridine (Ph-tpy; 1–3) or 4′-ferrocenyl-2,2′:6′,2′′-terpyridine (Fc-tpy; 4–6), N-O is the anion of 8-hydroxyquinoline (HQ in 1, 4), 5-chloro-7-iodo-8-hydroxyquinoline (CQ in 2, 5) or 5-nitro-8-hydroxyquinoline (NQ in 3, 6). The complex [Cu(Fc-tpy)₂](ClO₄)₂ (7) has also been prepared as a control and structurally characterized. The optimized geometries and the frontier orbitals of the complexes have been obtained from DFT calculations. The ferrocenyl appended complexes having the anticancer active CQ (in 5) and NQ (in 6) ligands show remarkable cytotoxicity, giving the respective IC₅₀ values of 0.75 μM and 0.52 μM in HeLa and 1.3 μM and 2.6 μM in MCF-7 cancer cells. The phenyl appended complexes 2 and 3 are less active than their ferrocenyl analogues in both the cells while the complexes of HQ (in 1, 4) are the least active. Interestingly, complexes 4–6 are significantly less toxic to MCF-10A normal cells. The DCFDA, annexin-V-FITC and propidium iodide nuclear staining assays reveal an apoptotic mechanism of cell death which is attributable to the metal-assisted generation of reactive oxygen species. Imaging experiments on HeLa cells reveals that complex 5 accumulates primarily inside the mitochondria. The complexes bind to calf thymus DNA with moderate affinity giving K_b values in the range of 6.3 × 10⁴–7.4 × 10⁴ M⁻¹ and to HSA protein with significant affinity giving K_HSA values in the range of 8.6 × 10⁴–1.3 × 10⁵ M⁻¹. Their affinity for DNA suggests that mitochondrial DNA could be the target while their affinity for HSA suggests that they could be transported by HSA in the blood. This work is the first report to show that the ferrocenyl appended copper(II) complexes of hydroxyquinoline ligands are remarkably cytotoxic to cancer cells but significantly less toxic to normal cells.

First-principles density functional theory (DFT) calculations were carried out to investigate the structural and electronic properties of beryllium (Be) doped and, Be with boron (B) co-doped graphene systems.

First-principles density functional theory (DFT) based calculations were carried out to investigate the structural and electronic properties of beryllium and nitrogen co-doped and BeN/BeO molecules-doped graphene systems.

A series of four novel neodymium(III) complexes of the formulation [Nd(R-tpy)(O–O)(NO₃)₂] (1–4), where R-tpy is 4′-phenyl-2,2′:6′,2′′-terpyridine (Ph-tpy; 1, 2) and 4′-ferrocenyl-2,2′:6′,2′′-terpyridine (Fc-tpy; 3, 4); O–O is the conjugate base of acetylacetone (Hacac; 1, 3) or curcumin (Hcurc; 2, 4), are synthesized and characterized. The single crystal structure of 1 shows that the complex is a discrete mononuclear species with the Nd(III) centre in a nine coordinate environment provided by a set of O₆N₃ donor atoms. Complexes 1 and 3 having the simple acac ligand are prepared as control compounds. Complex 4, possessing an appended ferrocenyl (Fc) and the curcumin moiety, is remarkably photocytotoxic to HeLa and MCF-7 cancer cells in visible light giving respective IC₅₀ values of 0.7 μM and 2.1 μM while being significantly less toxic to MCF-10A normal cells (IC₅₀ = 34 μM) and in the dark (IC₅₀ > 50 μM). The phenyl appended complex 2, lacking a ferrocenyl moiety, is significantly less toxic to both the cell lines when compared with 4. Complexes 1 and 3, lacking the photoactive curcumin moiety, do not show any apparent toxicity both in light and in the dark. The cell death is apoptotic in nature and is mediated by the light-induced formation of reactive oxygen species (ROS). Fluorescence imaging experiment with HeLa cells reveals mitochondrial accumulation of complex 4 within 4 h of incubation. The complexes bind to calf thymus (ct) DNA with moderate affinity giving K_b values in the range of 10⁴–10⁵ M⁻¹. The curcumin complexes 2 and 4 cleave plasmid supercoiled DNA to its nicked circular form in visible light via¹O2 and ˙OH pathways. The presence of the ferrocenyl moiety is likely to be responsible for the enhanced cellular uptake and photocytotoxicity of complex 4. Thus, the mitochondria targeting complex 4, being remarkably cytotoxic in light but non-toxic in the dark and to normal cells, is a potential candidate for photochemotherapeutic applications.

An iron(iii)–Schiff base complex derived from vitamin B₆and thiosemicarbazide is significantly photocytotoxic to HeLa cancer cells in visible light (400 nm–700 nm) but non-toxic in the absence of light.