Abstract
Freshwater systems are faced with a myriad of stressors including geomorphological alterations, nutrient overloading and pollution. Previous studies in marine fish showed polyaromatic hydrocarbons (PAHs) to be cardiotoxic. However, the cardiotoxicity of anthropogenic pollutants in freshwater fishes is unclear and has not been examined across multiple levels of cardiac organization. Here we investigated the effect of phenanthrene (Phe), a pervasive anthropogenic pollutant on a sentinel freshwater species, the brown trout (Salmo trutta). We first examined the electrical activity of the whole heart and found prolongation (∼8.6%) of the QT interval (time between ventricular depolarization and repolarization) of the electrocardiogram (ECG) and prolongation (∼13.2%) of the monophasic action potential duration (MAPD) following ascending doses of Phe. At the tissue level, Phe significantly reduced trabecular force generation by ∼24% at concentration 15 μM and above, suggesting Phe reduces cellular calcium cycling. This finding was supported by florescent microscopy showing a reduction (∼39%) in the intracellular calcium transient amplitude following Phe exposure in isolated brown trout ventricular myocytes. Single-cell electrophysiology was used to reveal the mechanism underlying contractile and electrical dysfunction following Phe exposure. A Phe-dependent reduction (∼38%) in the L-type Ca2+ current accounts, at least in part, for the lowered Ca2+ transient and force production. Prolongation of the MAPD and QT interval was explained by a reduction (∼70%) in the repolarising delayed rectifier K+ current following Phe exposure. Taken together, our study shows a direct impact of Phe across multiple levels of cardiac organization in a key freshwater salmonid.
Highlights
We show changes in whole heart electrical activity consistent with arrhythmogenesis due to prolongation of the monophasic action potential duration (MAPD) and interval between ventricular depolarization and repolarization (QT interval) as shown in the electrocardiogram (ECG)
A representative MAP trace from an isolated heart (Fig. 1C) shows the effects of Phe on the MAP which reveals the time course of an action potential taken from the surface of the heart
We investigated the impact of a prevalent anthropogenic polyaromatic hydrocarbons (PAHs) pollutant, Phe, on cardiac function in a sentinel fresh water salmonid, the brown trout
Summary
Increase in global demand means increased production and transport of oil and oil-based products which has led to disasters within the aquatic environment. Major oil spills, such as the 1989 Exxon Valdez and the 2010 Deepwater Horizon disasters, released large quantities of hydrocarbons including large amounts of polyaromatic hydrocarbons (PAHs) into the aquatic ecosystem. Aside from spills, PAHs are an ever increasing anthropogenic pollutant in the aquatic environment constantly receiving input through atmospheric deposition of exhaust particles, soot from vehicular emissions, industrial emissions and forest fires (Lima et al, 2003; National Research Council (US) Committee on Oil in the Sea, 2003; Van Metre and Mahler, 2003; Brette et al, 2017; Thompson et al, 2017). Most worrisome is the fact that PAHs are persistent organic pollutants (Behera et al, 2018) and are known to cause a myriad of effects in a wide range of organisms including carcinogenicity (Baars, 2002; Laffon et al, 2006; Moorthy et al, 2015), disruption of the endocrine system (Gentes et al, 2007; Zhang et al, 2016), DNA damage and adduct formation (Hazilawati et al, 2017), developmental toxicity (Incardona et al, 2006; Carls et al, 2008; Li et al, 2011; Sorhus et al, 2016) and cardiotoxicity (Incardona et al, 2009, 2015; Zhang et al, 2013a, 2013b; Brette et al, 2014, 2017; Edmunds et al, 2015)
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