Graphene and its derivatives are an emerging class of
carbon nanomaterial with great potential for a broad range of industrial and consumer applications. However, their increasing production and use is expected to result in release of nano-sized
graphene platelets into the environment, where they may interact with chemical
pollutants modifying their fate and toxic potential. The objective of this study was to assess whether
graphene nanoplatelets can act as vector for aromatic
environmental pollutants increasing their cellular uptake and associated hazardous effects in vitro. For this purpose, cell cultures of the topminnow fish (Poeciliopsis lucida)
hepatoma cell line PLHC-1 were simultaneously (and successively) exposed to
graphene nanoplatelets (
graphene oxide (GO) or carboxyl
graphene (CXYG)) and an
aryl hydrocarbon receptor (AhR) agonist (β-naphthoflavone (β-NF),
benzo(k)fluoranthene (BkF) or 3,3',4,4',5,5'-hexachlorobiphenyl (
PCB169)). Following exposure
cytochrome P450 1A (Cyp1A) induction was assessed by measuring cyp1A
mRNA expression levels using
reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR) and Cyp1A-dependent
ethoxyresorufin-O-deethylase (
EROD) activity. It was observed that pre- and co-exposure of cells to GO and CXYG nanoplatelets had a potentiating effect on β-NF, BkF, and PCB169-dependent Cyp1A induction suggesting that
graphene nanoplatelets increase the effective concentration of AhR agonists by facilitating their passive diffusion into the cells by damaging the cells' plasma membrane and/or by transporting them over the plasma membrane via a Trojan horse-like mechanism. The results demonstrate the existence of combination effects between nanomaterials and
environmental pollutants and stress the importance of considering these effects when evaluating their respective hazard.