2008-aquatic toxicology-evidence for multiple mechanisms of toxicity in larval rainbow.pdf
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2008-aquatic toxicology-evidence for multiple mechanisms of toxicity in larval rainbow
Aquatic Toxicology 88 (2008) 200–206
Contents lists available at ScienceDirect
Aquatic Toxicology
j o u rn al h omepage: www.elsevi er.c om /locate/aq uatox
Evidence for multiple mechanisms of toxicity in larval rainbow
trout (Oncorhynchus mykiss) co-treated with retene
and -naphthoflavone
Jason A. Scott, Peter V. Hodson ∗
Department of Biology, Queen’s University, 116 Barrie Street, Kingston, Ont. K7L 3N6, Canada
a r t i c l e i n f o a b s t r a c t
Article history: Alkylated polycyclic aromatic hydrocarbons, such as retene (7-isopropyl-1-methylphenanthrene), induce
Received 6 March 2008 cytochrome P450 1A (CYP1A) enzymes and produce dioxin-like toxicity in the embryo–larval stages of fish
Received in revised form 9 April 2008 characterized by the signs of blue sac disease (BSD). The signs of toxicity are well characterized; however,
Accepted 11 April 2008
the mechanism is not well understood. To elucidate the role of CYP1A in retene toxicity, larval rainbow
trout (Oncorhynchus mykiss) were co-treated with a range of concentrations of -naphthoflavone (ANF), a
Keywords: known CYP1A inhibitor. The co-treatment produced synergistic toxicity at 3.2–100 g/L ANF, after which
Retene
toxicity at 180 g/L ANF dropped to levels typical of retene-only. At 320 g/L ANF, toxicity increased with
-Naphthoflavone
Mechanisms or without retene, indicating that
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