Graphene-based nanomaterials received attention from scientists due to their unique properties: they are highly conductive, mechanically resistant and elastic. These materials can be used in different sectors of society from electronic energy storage in industry to biomedical applications. This study evaluates the influence of graphene nanoplatelets in vitro and in vivo. The toxicological influence of graphene nanoplatelets (GPs) was analyzed by cytotoxic methods, the change of cell proliferation was assessed in real-time, and the effect of GPs on a living organism was evaluated in an animal model using histopathological examination. We analyzed two types of GP administration: intratracheal and peroral. We found dose- and time-dependent cytotoxic effects of GPs in vitro; the concentration above 50 μg/mL increased the cytotoxicity significantly. The real-time analysis confirmed these data; the cells exposed to a high concentration of GPs for a longer time period resulted in a decrease in cell index which indicated lower cell viability. Histopathological examination revealed thickened alveolar septa and accumulation of GPs in the endocardium after intratracheal exposure. Peroral administration did not reveal any morphological changes. This study showed the dose- and time-dependent cytotoxic potential of graphene nanoplatelets in in vitro and in vivo models.

Earliest cells of neural lineage express pluripotency and early neural genes. However, conditions essential for propagating these cells are not known. In this study, we investigated several factors that would support and propagate embryonic stem cells (ES) derived early neural stem cells. RT-qPCR data revealed that PD325901 (MEK inhibitor), Leukemia inhibitory factor (LIF) and KN93 (CAMKII inhibitor) (henceforth referred as PLK media) upregulated expression of early neural genes Sox1 and Pax6 in ES cells, while the expression of pluripotency genes Oct4, Sox2 and Nanog remained on par with the ES cells cultured in ES media. On repeated passaging in PLK medium, expression of Sox1 and Pax6 increased gradually while expression of pluripotency genes remained constant. Moreover, even after several passages the PLK cultured cells were pluripotent, as confirmed by embryoid body (EB) mediated assay. To best of our knowledge, ours is the first group to report this unique combination of factors that potentially upregulated early neural genes while maintaining pluripotency. We feel it is appropriate to call the newly isolated cells “pro-neurogenic ES cells” (pnESC) and not primitive neural stem cells (pNSCs) since they retained pluripotency while pNSCs are not pluripotent.