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  • According to average serum fat


    According to average serum fat content of 6.9 g/L (Phillips et al., 1989) and serum dioxin level from individuals exposed to dioxins as the result of accidents in Seveso (Needham et al., 1997), Taiwan (Guo et al., 2004) and Vietnam (The Tai et al., 2011) the median serum concentration of TCDD would be 10−10 M to 10−11 M. However, B0AT1 PCI-24781 mg was only induced by TCDD of higher concentrations (10−8 M). SLC6A19 expression is more sensitive, whose upregulation could be found upon TCDD treatment at 10−10 M to 10−7 M, which might be used as a potential biomarker for risk assessment of exposure to dioxin and dioxin-like compounds. We concluded that dioxin and dioxin-like compounds upregulate expression of a Na+-coupled NAA transporter, SLC6A19, via AhR, and stimulation of its protein, B0AT1, may contribute to interferences with the NAA uptake caused by exposure to the toxic substances in HepG2 cells. Sophisticated elaboration on detailed cell signaling pathways related to B0AT1 function and regulation by AhR agonists needs to be carried out in the future.
    Contribution and acknowledgements
    Materials and methods
    Acknowledgements The authors thank M. en C. Ma. Cecilia Aguilar Zacarias and M. en C. Jorge Alfonso Maciel Ruiz for technical support, as well as Dr. Jan Vondráček for critical review of the manuscript. Gerardo Vázquez Gómez is a doctoral student from Programa de Doctorado en Ciencias Biomédicas, Universidad Nacional Autónoma de México (UNAM) and received fellowship 324651 from Consejo Nacional de Ciencia y Tecnología (CONACyT). This research was supported by funding from PAPIIT (IN210111, IN208314 and IN204816) and CONACyTCB-2012/178860. The authors declare no competing financial interests or conflicts of interest.
    Introduction In recent decades, significant attention has been paid to the dioxins and dioxin-like compounds which can act as aryl hydrocarbon receptor agonists (AhR-agonists) (Shen et al., 2009, Hong et al., 2014). These compounds can bind to aryl hydrocarbon receptor, and induce the dioxin-like toxicity such as teratogenicity, carcinogenesis, and other toxic responses. Due to persistence and difficult degradation, dioxins and dioxin-like compounds could bioaccumulate and biomagnify in the food chains. Dioxins and dioxin-like compounds have strong adsorption ability on sediments. Therefore, sediments are recognized as potential repositories of dioxins and dioxin-like compounds, such as polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDDs), and polychlorinated dibenzofurans (PCDFs) (Hilscherova et al., 2000, Dévier et al., 2011). These compounds could affect the benthic community and release into aquatic environment (Qiao et al., 2006, Sudaryanto et al., 2011, Gao et al., 2015, Wang et al., 2016). In view of the environmental risks of these compounds, it is necessary to study the AhR-agonists in sediments. In order to characterize the AhR-agonistic risks of complex dioxins and dioxin-like compounds mixture, toxic equivalency factor (TEF) concept and relative potency (REP) concept have been established and revised by the World Health Organization (WHO) (Van den Berg et al., 1998, Van den Berg et al., 2006). Based on TEF/REP values and chemical analysis, the total toxic potency of these mixtures could be expressed as chemically derived 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (Chem-TEQs), which are identified as significant indicators in the evaluation of ecological risk (Villeneuve et al., 2002). However, chemical analysis is short of the information of potential adverse biological effects (Qiao et al., 2006). In vitro bioassay can be used to characterize the overall potency of a mixture of dioxins and dioxin-like compounds. Previous studies have shown that in vitro ethoxyresorufin-O-deethylase (EROD) induction in the H4IIE cell bioassay is a sensitive biomarker and an effective method to characterize the AhR-agonistic potency of dioxins and dioxin-like compounds mixture (Keiter et al., 2008, Hong et al., 2012). The responses can be expressed as bioassay-derived 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (Bio-TEQs). Therefore, the combination of chemical analysis and in vitro bioassay is helpful for a comprehensive evaluation of the potency of AhR-agonist activity.