Carbon-encapsulated iron nanoparticles (CEINs) are emerging as promising biomedical tools due to their unique physicochemical properties. In this study, the cytotoxic effect of CEINs (the mean diameter distribution ranges 46–56 nm) has been explored by MTT, LDH leakage, Calcein-AM/propidium iodide (PI) and Annexin V-FITC/PI assays in human melanoma (HTB-140), mouse melanoma (B16-F10) cells, and human dermal fibroblasts (HDFs). The results demonstrated that CEINs produce mitochondrial and cell membrane cytotoxicities in a dose (0.0001–100 μg/ml)-dependent manner. Moreover, the studies elucidated some differences in cytotoxic effects between CEINs used as raw and purified materials composing of the carbon surface with acidic groups. Experiments showed that HTB-140 cells are more sensitive to prone early apoptotic events due to raw CEINs as compared to B16-F10 or HDF cells, respectively. Taken together, these results suggest that the amount of CEINs administered to cells and the composition of CEINs containing different amounts of iron as well as the carbon surface modification type is critical determinant of cytotoxic responses in both normal and cancer (melanoma) cells.Electronic supplementary materialThe online version of this article (doi:10.1007/s11051-013-1835-7) contains supplementary material, which is available to authorized users.
Carbon-encapsulated iron nanoparticles (CEINs) have been considered as attractive candidates for several biomedical applications. In the present study, we synthesized CEINs (the mean diameter 40-80 nm) using a carbon arc route, and the as-synthesized CEINs were characterized (scanning and transmission electron microscopy, dynamic light scattering, turbidimetry, Zeta potential) and further tested as raw and purified nanomaterials containing the carbon surface modified with acidic groups. For cytotoxicity evaluation, we applied a battery of different methods (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, lactate dehydrogenase, calcein AM/propidium iodide, annexin V/propidium iodide, JC-1, cell cycle assay, Zeta potential, TEM and inductively coupled plasma mass spectrometry) to address the strategic cytotoxic endpoints of Lewis lung carcinoma cells due to CEIN (0.0001-100 µg ml(-1) ) exposures in vitro. Our studies evidence that incubation of Lewis lung carcinoma cells with CEINs is accompanied in substantial changes of zeta potential in cells and these effects may result in different internalization profiles. The results show that CEINs increased the mitochondrial and cell membrane cytotoxicity; however, the raw CEIN material (Fe@C/Fe) produced higher toxicities than the rest of the CEINs studied to data. The study showed that non-modified CEINs (Fe@C/Fe and Fe@C) elevated some pro-apoptotic events to a greater extent compared to that of the surface-modified CEINs (Fe@C-COOH and Fe@C-(CH2 )2 COOH). They also diminished the mitochondrial membrane potentials. In contrast to non-modified CEINs, the surface-functionalized nanoparticles caused the concentration- and time-dependent arrest of the S phase in cells. Taken all together, our results shed new light on the rational design of CEINs, as their geometry, hydrodynamic and, in particular, surface characteristics are important features in selecting CEINs as future nanomaterials for nanomedicine applications.
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