BackgroundEngineered nanomaterials display unique properties that may have impact on human health, and thus require a reliable evaluation of their potential toxicity. Here, we performed a standardized in vitro screening of 23 engineered nanomaterials. We thoroughly characterized the physicochemical properties of the nanomaterials and adapted three classical in vitro toxicity assays to eliminate nanomaterial interference. Nanomaterial toxicity was assessed in ten representative cell lines.ResultsSix nanomaterials induced oxidative cell stress while only a single nanomaterial reduced cellular metabolic activity and none of the particles affected cell viability. Results from heterogeneous and chemically identical particles suggested that surface chemistry, surface coating and chemical composition are likely determinants of nanomaterial toxicity. Individual cell lines differed significantly in their response, dependent on the particle type and the toxicity endpoint measured.ConclusionIn vitro toxicity of the analyzed engineered nanomaterials cannot be attributed to a defined physicochemical property. Therefore, the accurate identification of nanomaterial cytotoxicity requires a matrix based on a set of sensitive cell lines and in vitro assays measuring different cytotoxicity endpoints.

As a part of a broader study directed towards helical coordination compounds with benzenedithiolate donors, we have synthesized the bis(benzenedithiol) ligands 1,2‐bis(2,3‐dimercaptobenzamido)ethane (H4‐1) and 1,2‐bis(2,3‐dimercaptophenyl)ethane (H4‐2). Both ligands form dinuclear complexes with NiII, NiIII and, after air‐oxidation, CoIII ions under equilibrium conditions. Complexes (NEt4)4[NiII2(1)2] (11 b), (NEt4)2[NiIII2(1)2] (13), and Na4[NiII2(2)2] (14) were characterized by X‐ray diffraction. In all complexes, two square‐planar [Ni(S2C6H3R)2] units are linked in a double‐stranded fashion by the carbon backbone and they assume a coplanar arrangement in a stairlike manner. Cyclic voltammetric investigations show a strong dependence of the redox potential on the type of the ligand. The substitution of 14− for 24− on nickel (−785 mV for 11 b versus −1130 mV for 14, relative to ferrocene) affects the redox potential to a similar degree as the substitution of nickel for cobalt (−1160 mV for [Co2(1)2]2−/[Co2(1)2]4−, relative to ferrocene). The redox waves display a markedly less reversible behavior for complexes with the shorter bridged ligand 24− compared to those of 14−.