title: Cytochrome P4501A1 is induced by PCB 77 and benzo[a]pyrene treatment but not by exposure to the Hudson River environment in Atlantic tomcod (Microgadus tomcod) post-yolk sac larvae.
abstract: In fish, the embryos and larvae are the life-stages most sensitive to damage from environmentally borne dioxin-like compounds and polycyclic aromatic hydrocarbons (PAHs). Methods are not routinely available to measure the body burdens of contaminants in embryos and larvae, thus precluding the investigation of links between exposure and biological effects. Quantification of expression of cytochrome P4501A1 (CYP1A1) provides an index of relative exposure of natural populations to bioavailable aromatic hydrocarbons (AH) and an initial evaluation of their biological effects. We developed a quantitative approach to standardize total RNA loading and then used competitive reverse transcriptase-polymerase chain reaction (RT-PCR) to quantify the CYP1A1 mRNA expression in environmentally exposed Atlantic tomcod (Microgadus tomcod) post yolk-sac larvae (postlarvae) from the Hudson River, New York, and in chemically treated postlarval offspring of controlled laboratory crosses of Hudson River parents. Significant induction of CYP1A1 expression was observed in tomcod postlarvae exposed to waterborne 3,3',4,4'-tetrachlorobiphenyl (PCB 77) (four-fold) and benzo[a]-pyrene (eight-fold) compared with vehicle-exposed controls. In contrast, CYP1A1 was not induced in Hudson River-exposed postlarvae compared with vehicle-exposed controls. This study demonstrates the feasibility of using competitive RT-PCR for the measurement of gene expression in environmentally exposed larvae of sentinel species, and is consistent with the hypothesis that postlarvae exposed to the Hudson River environment have not bioaccumulated sufficient levels of AHs to induce CYP1A1 expression. The high levels of hepatic CYP1A1 mRNA expression previously reported in 5-8 month old juvenile tomcod from the Hudson River coincides with their descent to the benthic habitat and the onset of independent feeding on AH-contaminated benthic prey.
authors.affiliation: Institute of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, New York 10987, USA.
authors.forename: Nirmal K
authors.initials: NK
authors.lastname: Roy
authors.forename: Simon
authors.initials: S
authors.lastname: Courtenay
authors.forename: Grace
authors.initials: G
authors.lastname: Maxwell
authors.forename: Zhanpeng
authors.initials: Z
authors.lastname: Yuan
authors.forename: R Christopher
authors.initials: RC
authors.lastname: Chambers
authors.forename: Isaac
authors.initials: I
authors.lastname: Wirgin
mesh_terms: D000818:Animals; D001564:Benzo(a)pyrene / Q000633:toxicity*; D019363:Cytochrome P-450 CYP1A1 / Q000096:biosynthesis / Q000235:genetics*; D004790:Enzyme Induction / Q000187:drug effects; D005399:Fishes; D005618:Fresh Water; D007814:Larva / Q000187:drug effects; D011078:Polychlorinated Biphenyls / Q000633:toxicity*; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014874:Water Pollutants, Chemical / Q000633:toxicity*
chemical_list: D012333:RNA, Messenger; D014874:Water Pollutants, Chemical; D001564:Benzo(a)pyrene; D011078:Polychlorinated Biphenyls; D019363:Cytochrome P-450 CYP1A1