Subchronic PAH Exposure Impacts Cardiac Electrophysiology of the Polar Fish, Navaga Cod (Eleginus nawaga)

Polycyclic aromatic hydrocarbons (PAHs) from the water-soluble fraction (WSF) of crude oil are recognized cardiotoxicants in fish; however, all electrophysiological evidence to date derives from acute exposure experiments. This study examined the effects of prolonged (5–8 h) incubation of isolated ventricular cardiomyocytes from the navaga cod (Eleginus nawaga, Walbaum, 1792) with 10% WSF (total dissolved tricyclic-PAH concentration in the tens-of-nM), 3 µM phenanthrene (Phe), or 3 µM 3-methylphenanthrene (3-MP) on action potential (AP) parameters and the underlying ionic currents using the whole-cell patch-clamp technique. WSF and 3-MP reduced AP amplitude and maximum rate of depolarization through suppression of the fast sodium current (INa), whereas Phe and 3-MP shortened AP duration, associated with decreased density and a hyperpolarizing shift in steady-state activation of the rapid delayed rectifier potassium current (IKr). The L-type calcium current and inward rectifier potassium current remained unaffected by all treatments. Notably, the effects of prolonged incubation differed qualitatively from previously reported acute responses to the same compounds, suggesting the involvement of indirect mechanisms such as reactive oxygen species production and activation of intracellular signaling cascades. These findings demonstrate that subchronic PAH exposure produces distinct and potentially proarrhythmogenic alterations in fish cardiac electrophysiology that cannot be predicted from acute exposure data alone.