Environmental polychlorinated biphenyl exposure and cytochromes P450 in raccoons (<i>Procyon lotor</i>)

  • Philip N. Smith
    The Institute of Environmental and Human Health, Texas Tech University/Texas Tech Health Sciences Center, Lubbock, Texas 79409–1163, USA
  • Stelvio M. Bandiera
    Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada
  • Sherry L. Skipper
    U.S. Fish and Wildlife Service, Rocky Mountain Arsenal NWR, Commerce City, Colorado 80022, USA
  • Kevin A. Johnson
    Southern Illinois University at Edwardsville, Edwardsville, Illinois 62026–1652, USA
  • Scott T. McMurry
    The Institute of Environmental and Human Health, Texas Tech University/Texas Tech Health Sciences Center, Lubbock, Texas 79409–1163, USA

説明

<jats:title>Abstract</jats:title> <jats:p>An investigation involving raccoons as a sentinel species at the Paducah Gaseous Diffusion Plant (PGDP) and Ballard Wildlife Management Area in western Kentucky (USA) delineated the extent of exposure to polychlorinated biphenyls (PCBs). Three separate measures of hepatic cytochrome P450 (CYP) induction were used to evaluate raccoon physiological responses to PCB exposure. Hepatic CYP induction was estimated via determination of total CYP, dealkylase activities, and immunoreactive proteins. There were no differences in raccoon biomarker responses between study sites. Significant relationships between and among PCB residues and biomarkers indicated that hepatic CYP induction had occurred in response to PCB exposure. Pentoxy-resorufin O-deethylase (PROD) activity, CYP1A1, and CYP1A2 were biomarkers most closely associated with PCB exposure. The rank order of responses was CYP1A1 &gt; CYP1A2 &gt; PROD &gt; ethoxyresorufin O-deethylase (EROD) as related to raccoon liver PCB concentrations, whereas the order was CYP1A1 &gt; PROD &gt; EROD &gt; CYP1A2 when regressed with total PCB concentrations in abdominal fat.</jats:p>

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