Effects of Phenanthrene on Electrical Activity of Ventricular Cardiomyocytes in Atlantic Cod (Gadus morhua)

Abstract

Oil production in the Arctic shelf and its shipping via the Northern Sea Route increase risks of pollution of Arctic ecosystems with oil and its products. Polyaromatic hydrocarbons are known to be the most toxic oil components, with phenanthrene being the most abundant among them and causing the most robust effects. Phenanthrene is known for its high toxicity for developing fish hearts, with its cardiotoxic effects being species-specific. Meanwhile, the effects of phenanthrene on cardiac function in Arctic fish, including commercially important fish species, are still poorly understood. Here, we studied the effects of phenanthrene on electrical activity and ionic currents in isolated ventricular cardiomyocytes of the Atlantic cod (Gadus morhua) using the patch clamp technique. The major ionic currents in cod myocardium were I_Kr, I_K1, I_Na and I_Ca. Phenanthrene at a concentration of 1 µM (1) had no effect on the duration of action potentials (APs), (2) suppressed rapid delayed rectifier K⁺ current I_Kr by 61.33 ± 3.94%, thus decreasing the repolarization reserve in cardiomyocytes, (3) had no effect on either the resting potential level or background inward rectifier K⁺ current (I_K1), (4) decreased AP upstroke velocity due to suppression of fast Na⁺ current (I_Na), (5) insignificantly reduced the amplitude of Ca²⁺ current (I_Ca) and accelerated its inactivation, which overall led to a decrease in I_Ca total cumulative charge transfer. Thus, the effects of phenanthrene on cod myocardium at a cellular level can be characterized as potentially proarrhythmic, which makes cod populations in the Arctic seas vulnerable to pollution of the aquatic environment with toxic oil components during oil spills in the event of man-made disasters.