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Polluted-site killifish (Fundulus heteroclitus) embryos are resistant to organic pollutant-mediated induction of CYP1A activity, reactive oxygen species, and heart deformities

Authors

  • Xabier Arzuaga,

    Corresponding author
    1. Graduate Center for Toxicology, 306 Health Sciences Research Bulding, Lexington, Kentucky 40536-0305, USA
    2. Department of Biology, 101 Morgan Building, University of Kentucky, Lexington, Kentucky 40506, USA
    Current affiliation:
    1. U.S. Environmental Protection Agency, National Center for Environmental Assessment, Office of Research and Development, Mail Code: 8601P, 1200 Pennsylvania Ave, NW, Washington, DC 20460, USA.
    • Graduate Center for Toxicology, 306 Health Sciences Research Bulding, Lexington, Kentucky 40536-0305, USA.
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  • Adria Elskus

    1. Graduate Center for Toxicology, 306 Health Sciences Research Bulding, Lexington, Kentucky 40536-0305, USA
    2. Department of Biology, 101 Morgan Building, University of Kentucky, Lexington, Kentucky 40506, USA
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Abstract

Exposure to coplanar polychlorinated biphenyls (PCBs) and polycyclic aromatic hydrocarbons (PAHs) can adversely affect fish embryonic development, induce expression of cytochrome P4501A (CYP1A), and increase reactive oxygen species (ROS) production, effects believed to be mediated by the aryl hydrocarbon receptor (AHR). Killifish (Fundulus heteroclitus) populations in New Bedford Harbor, Massachusetts, USA (NBH) and Newark Bay, New Jersey, USA (NB) are generationally exposed to coplanar PCBs and PAHs and have developed resistance to PCB mediated induction of CYP1A. We hypothesized that fish resistant to CYP1A induction would also exhibit resistance to PCB and PAH induced ROS production and teratogenesis. Killifish embryos from two contaminated (NB, NBH) and two reference-site populations were exposed to vehicle or 3,3′4,4′5-pentachlorobiphenyl (PCB126) or 3-methylcholanthrene (3-MC) and evaluated for in ovo CYP1A activity, heart deformities, and ROS production. Both chemicals significantly increased in ovo ethoxyresorufin-O-deethylase (EROD) and ROS production in reference-site embryos. These chemicals provoked only moderate induction of in ovo EROD in NBH and NB embryos, and neither PCB126 nor 3-MC induced ROS production in these populations. Similarly, heart deformities were significantly induced by PCB126 in reference-site embryos, but had no significant effects on NB and NBH animals. These results indicate that fish resistant to CYP1A induction also exhibit decreased sensitivity to PCB126 and 3-MC-induced ROS production and teratogenesis. These findings further our understanding of toxicant resistance by demonstrating that reduced response to coplanar PCBs and PAHs extends beyond resistance to CYP1A induction to resistance to the physiological and teratogenic effects of these toxicants, responses that undoubtedly contribute to the increased survival of killifish inhabiting contaminated sites. Environ. Toxicol. Chem. 2010;29:676–682. © 2009 SETAC

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