Phenanthrene alters the electrical activity of atrial and ventricular myocytes of a polar fish, the Navaga cod.

Oil and gas exploration in the Arctic can result in the release of polycyclic aromatic hydrocarbons (PAHs) into relatively pristine environments. Following the recent spill of approximately 17 500 tonnes of diesel fuel in Norilsk, Russia, May 2020, our study focussed on the effects of phenanthrene, a low molecular weight PAH found in diesel and crude oil, on the isolated atrial and ventricular myocytes from the heart of the polar teleost, the Navaga cod (Eleginus nawaga). Acute exposure to phenanthrene in navaga cardiomyocytes caused significant action potential (AP) prolongation, confirming the proarrhythmic effects of this pollutant. We show AP prolongation was due to potent inhibition of the main repolarising current, I(Kr), with an IC(50) value of ~2 µM. We also show a potent inhibitory effect (~55%) of 1 µM phenanthrene on the transient I(Kr) currents that protects the heart from early-after-depolarizations and arrhythmias. These data, along with more minor effects on inward sodium (I(Na)) (~17% inhibition at 10 µM) and calcium (I(Ca)) (~17% inhibition at 30 µM) currents, and no effects on inward rectifier (I(K1) and I(KAch)) currents, demonstrate the cardiotoxic effects exerted by phenanthrene on the atrium and ventricle of navaga cod. Moreover, we report the first data that we are aware of on the impact of phenanthrene on atrial myocyte function in any fish species.