High temperature and hyperkalemia increase vulnerability of navaga cod (Eleginus nawaga) cardiomyocytes to the ecotoxicant 3-methyl-phenanthrene.

Oil and gas mining and transportation in the Arctic can lead to release of polycyclic aromatic hydrocarbons (PAHs) in the ocean and freshwater basins. PAHs are known for their toxic effects in fish hearts, including the inhibition of main ionic currents (I, I and I) in fish cardiac myocytes. The present study is the first one to assess the effect of a particular PAH abundant in crude oil and diesel, namely 3-methyl-phenanthrene (3-MP), on the electrical excitability (EE) of cardiomyocytes from navaga cod (Eleginus nawaga), commercial fish species from the Arctic. Action potentials (APs) were elicited in current-clamp experiments at 9, 15 and 21 °C, and AP characteristics and the current needed to elicit APs were examined. Also, the effects of 3 μM 3-MP were tested at 3 temperatures and in normal (3.5 mM) and high (8 mM) extracellular K concentrations. Elevation of temperature leads to hyperpolarization of resting membrane potential and AP shortening, but does not decrease EE. 3-MP was found to suppress EE in cardiomyocytes at 9 and 15 °C, but not at 21 °C. High extracellular K itself drastically decreases EE, although it does not worsen the effect of 3-MP. However, combination of hyperthermia and high K leads to augmentation of depressive effect of 3-MP on EE. We hypothesize that hyperthermia rescues Na channels from inactivation due to membrane hyperpolarization, thereby compensating for the partial inhibition of I by 3-MP. However, elevation of extracellular K nullifies this protective mechanism by depolarizing the resting potential and aggravates the effect of 3-MP.