| pubmed-article:16268147 | pubmed:abstractText | A suppression of hepatic ethoxyresorufin-O-deethylase (EROD) activity was reported recently in large-sized Atlantic tomcod (Microgadus tomcod) from the St. Lawrence Estuary (SLE; QC, Canada), possibly related to chronic exposure to persistent contaminants and/or to emaciation. In the present study, hepatic concentrations of organochlorine contaminants and biological responses were measured in female tomcods from three estuaries located on the Canadian east coast: The SLE, the Miramichi (ME), and the Richibucto (RE) Rivers Estuaries (NB, Canada). Tomcods from the SLE had higher hepatic concentrations of organochlorine contaminants than tomcods from the ME and RE. For example, concentrations of polychlorinated biphenyls (PCBs, lipid wt) were 2.5 to 4 times higher, and concentrations of mirex and chlordanes were 6 times higher, in tomcods from the SLE than in tomcods from the other sites. Concentrations of polycyclic aromatic hydrocarbons (PAHs) metabolites in the bile did not differ among sites. The pattern of biological responses differed markedly between the SLE and the two other sites. Tomcods from the SLE had 1.5 times higher concentrations of DNA adducts and 2 times higher rates of hepatocellular proliferation, but 20 times lower hepatic EROD activity, than tomcods from the ME and RE. Lipid content was not correlated with EROD activity, indicating that low hepatic lipid content alone does not cause suppression of EROD activity in Atlantic tomcod. In contrast, for the three sites combined, EROD activity decreased as concentrations of PCBs increased. Within sites, hepatic PCB concentrations increased as lipid content decreased. This study supports the hypothesis that low EROD activity in SLE tomcods is related to chronic exposure to organochlorine contaminants. | lld:pubmed |
