Approved Abstracts

Graphene oxide potentiates cytochrome P450 (CYP) induction caused by benzo-k-fluoranthene (BkF) in vitro



Author(s): Valdehita A; Fernández-Cruz ML; Navas JM;
Presenter: José Mª Navas

The increasing use of Graphene oxide (GO) will result in its release into the environment being essential to determine its final fate. The objective of the present work was to observe a possible role of the aryl hydrocarbon receptor (AhR) dependent cytochrome P4501A (CYP1A) on the catabolism of GO. Our hypothesis of work is that GO cannot initially interact with AhR, but that after an initial degradation caused by other mechanisms, small fractions of GO could activate AhR inducing CYP1A. The environmental pollutant BkF was used to provoke the initial activation of Ahr. A rainbow trout (Oncorhynchus mykiss) cell line was used in exposure experiments. CYP1A induction was monitored by measuring Ethoxyresorufin-O-deethylase (EROD) activity.
The co-exposure of cells to GO and BkF had a potentiating effect on BkF dependent CYP1A induction both at enzymatic and mRNA expression level. The obtained results suggest a possible role for the AhR and CYP1A system on the cellular metabolism of GO. The results also demonstrate that the presence of the GO could enhance the toxicity of environmental pollutants
This research was supported by the European Union's Horizon 2020 Graphene Flagship Core Project 2 programme


Keywords: Graphene Oxide; EROD activity; aryl hydrocarbon receptor

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