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Abstract
The present project assessed the effect of environmental contamination with polychlorinated dibenzo‐p‐dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs) on hepatic microsomal ethoxyresorufin O‐deethylase (EROD) activities and morphological parameters in matched double‐crested cormorant (Phalacrocorax auritus) hatchlings from egg clutches chosen for chemical analysis. Double‐crested cormorant eggs were collected from five colonies across Canada, with differing levels of contamination. Levels of contamination expressed in sum of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin‐toxic equivalents (TCDD‐toxic equivalents or TEQ, ng/kg egg; mean ± SEM) were: Saskatchewan, 250 ± 50; Chain Islands, 672 ± 73; Christy Islet, 276 ± 14; Crofton, 131, n = 1; and Lake Ontario, 1606 ± 118. In the hatchlings, hepatic EROD activities (pmol/min/mg protein; mean ± SEM) were: Saskatchewan, 283 ± 42; Chain Islands, 516 ± 98; Christy Islet, 564 ± 91; Crofton, 391 ± 52; and Lake Ontario, 2250 ± 156. Hepatic microsomal EROD activity (pmol/min/mg protein) regressed positively on TEQ (r2 = .69; p < .00005; n = 25). Yolk weight (g) regressed negatively on TEQ (r2 = .44; p = .00005). Wing length (mm) regressed negatively on PCB‐169 (r2 = .28; p = .007). Monospecific antibodies raised against rat cytochrome P‐450 1A1 recognized a protein in the hepatic microsomes of the double‐crested cormorant, and also in those of the great blue heron (Ardea herodias), using immunoblotting. The intensity of the stained band increased with increased EROD activity, supporting the assumption that ethoxyresorufin is a suitable substrate for avian cytochrome P‐450 1A1. These results validate the use of avian hepatic microsomal EROD activity as an index of cytochrome P‐450 1A1 induction by environmental levels of polychlorinated aromatic hydrocarbons and as a useful screening tool to determine the extent of exposure to such chemicals. Furthermore, the induction of cytochrome P‐450 1A1 observed in the cormorant indicates that the Ah receptor‐mediated process, by which TCDD and related chemicals exert many of their toxicities, has been activated.