Epigenetic changes upon multi-residue exposure to polycyclic aromatic hydrocarbons.

Introduction Besides genetic mechanisms, rapidly growing evidences have linked environmental pollutants (e.g. polycyclic aromatic hydrocarbons, PAH), with epigenetic variations, including changes in DNA methylation among others [1]. Whether these changes are a response to DNA damage and/or a consequence of environment exposure needs to be further explored. To date, studies concerning the effect of PAH exposure on the global DNA methylation are limited and contradictory results have been observed [2-5]. The reported differences might be partially explained by the differences between single compound exposures, generally used for in vitro studies [2;3], and humans' environmental multi-residues exposure [4;5]. In this context, the present study was intended to study the epigenetic modification induced by multi-residue exposure to PAH, based on an animal model. Rats sub-chronically exposed to a mixture of 16 US-EPA priority PAH were used to assess the (hydroxyl)methylation status of genomic DNA and RNA, together with reduced and oxidized forms of glutathione.