Why the study?
Earlier studies showed negative effects of phenanthrene on fish heart function, but its cardiac electrophysiological effects in shorthorn sculpin needed elucidation.
Low concentrations of phenanthrene induce proarrhythmic electrophysiological changes in fish ventricular myocytes by suppressing potassium and sodium currents.
Phenanthrene disrupts cardiac electrophysiology in Arctic fish; leaves open relevance to human cardiotoxicity from oil pollutants.
Phenanthrene (Phen) is one of the widespread species of polyaromatic hydrocarbons, a tricyclic compound, component of crude oil and diesel fuel. Earlier studies have shown its negative effects on fish heart function that may explain the toxicity of this pollutant. The present study aimed to elucidate the cardiac electrophysiological effects of Phen in shorthorn sculpin, the widespread and common fish of the Arctic region using the patch-clamp technique. We have found pronounced effects of Phen on the duration and upstroke velocity of action potentials (APs) in sculpin ventricular myocytes. 1 µM Phen produced almost two-fold prolongation of AP duration measured at 90% repolarization level and significant reduction of maximal upstroke velocity of AP. These effects are attributed to suppression of K+ rapid delayed rectifier current IKr (IC50 = 144 nM) and fast Na+ current INa (IC50 = 5.85 µM). Resting membrane potential and K+ inward rectifier current IK1 were not affected by Phen even in the maximal concentration of 30 µM. Thus, low concentrations of Phen induce changes in cellular electrical activity of sculpin ventricular myocytes which might lead to proarrhythmic effects such as slowing of repolarization and decrease in excitation conduction velocity at the tissue level.
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Филатова et al. (2022) studied this question.
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