![]() However, polycyclic aromatic hydrocarbons (PAHs) and their alkylated homologues are believed to be the main bioavailable components that are toxic to developing fish 11, 12. Unlike other species studied to date, the haddock eggshell (chorion) binds oil droplets, enhancing exposure to toxic compounds within crude oil.Ĭrude oil is a complex chemical mixture containing hundreds of thousands of different compounds. ![]() We recently identified a unique susceptibility of haddock embryos to toxicity from dispersed crude oil 10. A baseline understanding of crude oil toxicity to these species is essential for regulatory decision making, spill response planning, and environmental risk assessment of oil production impacts in spawning and nursery habitats. Consequently, there is considerable political and public debate with respect to adverse impacts on these areas from either accidental oil spills or chronic exposure to operational discharges from oil platforms 5, 6, 7, 8, 9. Expansion of oil production in Northern Norway has been proposed for the Lofoten and Vesterålen regions, which are also crucial spawning and nursing grounds for three of the most important commercial fish species in the North Atlantic, including Atlantic haddock ( Melanogrammus aeglefinus), cod ( Gadus morhua) and herring ( Clupea harengus) 5. Oil spills in critical fish spawning habitats or aquaculture areas are a recurrent worldwide problem 1, 2, 3, 4. These data support a unifying hypothesis whereby depletion of intracellular calcium pools by crude oil-derived PAHs disrupts several pathways critical for organogenesis in fish. Furthermore, down-regulation of genes encoding specific components of the EC coupling machinery suggests that crude oil disrupts excitation-transcription coupling or normal feedback regulation of ion channels blocked by PAHs. The specific nature of the craniofacial abnormalities suggests that crude oil may target common craniofacial and cardiac precursor cells either directly or indirectly by affecting ion channels and intracellular calcium in particular. Because of oil droplet binding, a 24-hr exposure was sufficient to create severe cardiac and craniofacial abnormalities. We quantified effects on cardiac function and morphogenesis, characterized novel craniofacial defects, and examined the expression of genes encoding potential targets underlying cardiac and craniofacial defects. ![]() Using lower concentrations of dispersed crude oil (0.7–7 μg/L ∑PAH), here we exposed a broader range of developmental stages over both short and prolonged durations. We previously found that eggs of Atlantic haddock ( Melanogrammus aeglefinus) bind dispersed oil droplets, potentially leading to more profound toxic effects from uptake of polycyclic aromatic hydrocarbons (PAHs). Recent studies have shown that crude oil exposure affects cardiac development in fish by disrupting excitation-contraction (EC) coupling.
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