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Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous contaminants in aqueous environments. They affect cardiovascular development and function in fishes. The 3‐ring PAH phenanthrene has recently been shown to impair cardiac excitation–contraction coupling by inhibiting Ca2+ and K+ currents in marine warm‐water scombrid fishes. To see if similar events take place in a boreal freshwater fish, we studied whether the PAHs phenanthrene and retene (an alkylated phenanthrene) modify the action potential (AP) via effects on Na+ (INa), Ca2+ (ICaL), or K+ (IKr, IK1) currents in the ventricular myocytes of the rainbow trout (Oncorhynchus mykiss) heart. Electrophysiological characteristics of myocytes were measured using whole‐cell patch clamp. Micromolar concentrations of phenanthrene and retene modified the shape of the ventricular AP, and retene profoundly shortened the AP at low micromolar concentrations. Both PAHs increased INa and reduced ICaL and IKr, but retene was more potent. Neither of the PAHs had an effect on IK1. Our results show that phenanthrene and retene affect cardiac function in rainbow trout by a mechanism that involves multiple cardiac ion channels, and the final outcome of these changes (shortening of AP) is opposite to that observed in scombrid fishes (prolongation of AP). The results also show that retene and aryl hydrocarbon receptor (AhR) agonist have an additional mechanism of toxicity besides the previously known AhR‐mediated, transcription‐dependent one. Environ Toxicol Chem 2019;38:2145–2153. © 2019 SETAC.

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. (2016). Retene causes multifunctional transcriptomic changes in the heart of rainbow trout (Oncorhynchus mykiss) embryos. Environmental Toxicology and Pharmacology, 41, 95-102. doi:10.1016/j.etap.2015.11.015 hydrocarbons (PAHs). This study explored the cardiac transcriptome of rainbow trout (Oncorhynchus mykiss) eleuteroembryos exposed to retene, an AhR-agonistic PAH. The embryos were exposed to retene (nominal concentration 32 µg/L) and control, their hearts were collected before, at and after the onset of the visible signs of developmental toxicity, and transcriptomic changes were studied by microarray analysis.Retene up-or down-regulated 122 genes. The largest Gene Ontology groups were signal transduction, transcription, apoptosis, cell growth, cytoskeleton, cell adhesion/mobility, cardiovascular development, xenobiotic metabolism, protein metabolism, lipid metabolism and transport, and amino acid metabolism. Together these findings suggest that retene affects multiple signaling cascades in the heart of rainbow trout embryos, and potentially disturbs processes related to cardiovascular development and function.