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Aryl Hydrocarbon Receptor–Independent Toxicity of Weathered Crude Oil during Fish Development

Ecotoxicology and Environmental Fish Health Program, Environmental Conservation Division, Northwest Fisheries Science Center, National Oceanic and Atmospheric Administration, Seattle, Washington 98112, USA.
Environmental Health Perspectives (Impact Factor: 7.03). 01/2006; 113(12):1755-62. DOI: 10.1289/ehp.8230
Source: PubMed

ABSTRACT Polycyclic aromatic hydrocarbons (PAHs), derived largely from fossil fuels and their combustion, are pervasive contaminants in rivers, lakes, and nearshore marine habitats. Studies after the Exxon Valdez oil spill demonstrated that fish embryos exposed to low levels of PAHs in weathered crude oil develop a syndrome of edema and craniofacial and body axis defects. Although mechanisms leading to these defects are poorly understood, it is widely held that PAH toxicity is linked to aryl hydrocarbon receptor (AhR) binding and cytochrome P450 1A (CYP1A) induction. Using zebrafish embryos, we show that the weathered crude oil syndrome is distinct from the well-characterized AhR-dependent effects of dioxin toxicity. Blockade of AhR pathway components with antisense morpholino oligonucleotides demonstrated that the key developmental defects induced by weathered crude oil exposure are mediated by low-molecular-weight tricyclic PAHs through AhR-independent disruption of cardiovascular function and morphogenesis. These findings have multiple implications for the assessment of PAH impacts on coastal habitats.

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    • "Low molecular weight PAHs act preferentially through the narcosis pathway while high molecular weight PAHs involve binding to aryl hydrocarbon receptor AhR (Di Toro et al. 1991; Wassenberg and Di Giulio 2004). It has been recently demonstrated that three ring compounds can also act through an unknown AhR-independent pathway (Hawkins et al. 2002; Incardona et al. 2005). "
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    • "Thus, our observations of enlarged hearts, unlooped or improperly looped hearts, atrial and atrio-ventricular regurgitation, circulatory stasis, small eyes, and lack of swim bladder inflation are all consistent with cardiotoxicity caused by three-ring PAHs, with possible contributions from the higher molecular weight four-and five-ring PAHs as well (Goodale et al., 2013; Huang et al., 2012; Incardona et al., 2006, 2011; Zhang et al., 2012). Notably, the effects we observed here are very similar to those reported previously in zebrafish embryos exposed to crude oil-derived PAHs (Carls et al., 2008; Incardona et al., 2005; Jung et al., 2013). At a coarse level, therefore, the effects of PAHs on fish early life stages appear consistent irrespective of whether they originate from crude oil or refined petroleum that was subsequently burned in a combustion engine and deposited on urban roadways as motor vehicle exhaust (Bui et al., 2012). "
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