Perfluorooctane sulfonate (PFOS) is one of the most commonly used perfluorinated compounds, whose environmental exposure has been associated with a number of adverse health outcomes. However, the molecular mechanisms involved in PFOS toxicity are still not well elucidated. In the present study, we applied iTRAQ labeling quantitative proteomic technology to investigate the differential protein expression profiles of non-tumor human hepatic cells (L-02) exposed to PFOS. A total of 18 proteins were differentially expressed in a dose-dependent manner in PFOS-treated cells versus the control. Among these, 11 proteins were up-regulated and 7 were down-regulated. Gene ontology analysis indicated that PFOS would exert toxic effects on L-02 cells by affecting multiple biological processes, including protein biosynthesis and degradation, mRNA processing and splicing, transcription, signal transduction and transport. Furthermore, the proteomic results especially proposed that the inhibition of HNRNPC, HUWE1 and UBQLN1, as well as the induction of PAF1 is involved in the activation of the p53 and c-myc signaling pathways, which then trigger the apoptotic process in L-02 cells exposed to PFOS. Overall, these data will aid our understanding of the mechanisms responsible for PFOS-mediated hepatotoxicity, and develop useful biomarkers for monitoring and evaluating PFOS contamination in the environment.
Keywords: L-02 cell line; apoptosis; differential protein expression; iTRAQ; perfluorooctane sulfonate; proteomics.
Copyright © 2013 John Wiley & Sons, Ltd.