Is hepatic cytochrome P4501A1 expression predictive of hepatic burdens of dioxins, furans, and PCBs in Atlantic tomcod from the Hudson River estuary?
Hepatic cytochrome P4501A1 (CYP1A1) expression in fishes is frequently used to evaluate bioavailable aromatic hydrocarbon contamination of aquatic ecosystems. In controlled laboratory experiments, CYP1A1 expression in naïve fishes is usually dose-responsive to aromatic hydrocarbons and in field studies levels of gene expression in natural populations often correspond with known levels of sediment-borne contaminants. We quantified CYP1A1 mRNA levels in juvenile Atlantic tomcod Microgadus tomcod from 42 sites in the Hudson River estuary to evaluate the correspondence between hepatic CYP1A1 expression and hepatic concentrations of persistent halogenated aromatic hydrocarbons and to determine the utility of CYP1A1 expression as a biomarker in evaluating the microgeographic distribution of bioavailable contaminants within a large aquatic ecosystem. We found significant spatial heterogeneity in CYP1A1 mRNA levels among collection sites with levels of gene expression differing in some cases by 23-34 folds. CYP1A1 mRNA expression was highest in tomcod from the Newark Bay complex and lowest in tomcod from the most upriver collection sites in the main stem of the Hudson River. Although levels of PCDDs, PCDFs, and PCBs expressed as TCDD TEQs and CYP1A1 mRNA were highest in tomcod from the Newark Bay complex, there was no relationship between hepatic halogenated aromatic hydrocarbon levels and hepatic CYP1A1 mRNA in tomcod from sites in the main stem of the Hudson River. These results suggest that levels of CYP1A1 expression in fish from sites highly polluted with mixtures of halogenated aromatic hydrocarbons and other xenobiotics may not always be reflective of levels of bioavailable aromatic hydrocarbon contaminants. Based on these results and earlier controlled laboratory experiments, we hypothesize that elevated levels of CYP1A1 expression in tomcod from the Hudson River may be due primarily to PAHs or other contaminants not measured in this study.
Yuan
Z
Z
Institute of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987, USA.
Wirgin
M
M
Courtenay
S
S
Ikonomou
M
M
Wirgin
I
I
D000818:Animals; D001682:Biological Availability; D015415:Biomarkers; D019363:Cytochrome P-450 CYP1A1 / Q000096:biosynthesis*; D004147:Dioxins / Q000009:adverse effects*; D004781:Environmental Exposure; D005399:Fishes / Q000502:physiology*; D005663:Furans / Q000009:adverse effects*; D005786:Gene Expression Regulation; D008099:Liver / Q000187:drug effects* / Q000201:enzymology*; D011078:Polychlorinated Biphenyls / Q000009:adverse effects*; D014874:Water Pollutants, Chemical / Q000009:adverse effects*
D015415:Biomarkers; D004147:Dioxins; D005663:Furans; D014874:Water Pollutants, Chemical; D011078:Polychlorinated Biphenyls; D019363:Cytochrome P-450 CYP1A1