Impact of waterborne and trophic mercury exposures on cardiac function of two ecologically distinct Neotropical freshwater fish Brycon amazonicus and Hoplias malabaricus

Abstract

Metal pollutants have been considered one of the main factors underlying the depletion of biodiversity in natural populations unbalancing aquatic environments. The aim of this study was to evaluate the effects of exposure to inorganic Hg on myocardial contractility and the electrocardiogram (ECG) of two ecologically distinct Neotropical fish species, namely: matrinxã (Brycon amazonicus) and trahira (Hoplias malabaricus). Matrinxãs were exposed to a sublethal concentration of 0.1mgL of Hg in water for 96h. Trahiras were exposed to dietary Hg doses (0.45mg of Hg, each 4days, for 30days) using juvenile B. amazonicus as the prey vehicle. Hg exposures decreased myocardial isometric twitch force development, harmed contraction/relaxation dynamics and cardiac pumping capacity (CPC), and reduced the relative contribution of the calcium stored in the sarcoplasmic reticulum (SR) to excitation contraction (EC) coupling in both fish species. Analysis of the ECG revealed that Hg impaired electrical conduction across the heart, inducing first degree atrioventricular block and lengthening the plateau phase of action potential duration. In trahira trophic doses of Hg induced a marked bradycardia, increasing the duration of the ventricular action potential and delaying atrial and ventricular depolarization. These findings indicate that both acute and long-term Hg exposure, by different routes is cardiotoxic to matrinxã and trahira. Hg potently impaired intracellular calcium kinetics in the cardiomyocytes, myocardium contractility, and electrical conduction across the heart, all of which can be implicated in decreased cardiac output and putative heart failure.

Effects of change in temperature on the cardiac contractility of broad‐snouted caiman (Caiman latirostris) during digestion

“…The contribution of SR for Ca 2+ management at both temperatures was indirectly tested by a post‐rest contractile behavior, before and after adding RYA. Some mammalian and fish species exhibit a post‐rest potentiation of twitch force in response to diastolic pauses (Monteiro et al, 2017; Rivaroli et al, 2006; Rocha et al, 2007b; Vassallo & Mill, 1988). Post‐rest potentiation of contraction force has been related to the amount of Ca 2+ stored within and released from the SR (Bers, 1985; Edman & Jóhannsson, 1976; Rumberger & Reichel, 1972).…”

“…The force transducers were connected to an AECAD 04F amplifier (AVS Projetos) coupled to the acquisition data system (AQCAD 2.3.5; AVS Projetos). The preparations were stretched to provide a twitch tension at the maximum of the length–twitch tension relation (Kalinin & Gesser, 2002; Monteiro et al, 2017; Vasconcelos et al, 2020). Twitch tension was stabilized for about 30 min at 0.2 Hz before each protocol.…”

Selenium alleviates ER calcium depletion-induced endoplasmic reticulum stress dependent apoptosis via PERK/ATF4/CHOP pathway in chicken myocardium after mercuric chloride exposure

“…Ca 2+ regulates important physiological and pathological processes in cells in a concentration-dependent manner, but how it is involved in the myocardial cytotoxicity of HgCl 2 remains outstanding. A recent study demonstrated that HgCl 2 impaired the regulation of cytoplasmic Ca 2+ concentration by ER in cardiomyocytes (Monteiro et al 2017), which prompted us to evaluate this event initially. The results showed that the protein expression of SERCA2 was decreased while that of its inhibitory substrate PLN was increased in the HgCl 2 group compared to the Con group (Fig.…”

Use of complex physiological traits as ecotoxicological biomarkers in tropical freshwater fishes

“…This may indicate direct toxic effects on cardiac myocytes. Several studies have reported decreased myocardial isometric twitch force development in tropical fishes exposed to pollutants (de Andrade Waldemarin et al, 2012; Incardona et al, 2004; Monteiro et al, 2017; Thomaz et al, 2009). Reduced cardiac performance can increase the likelihood of starvation, predation vulnerability, and disease susceptibility (Incardona & Scholz, 2017).…”