The mechanisms of cardiac contraction impairment in salmonids by silver nanoparticles

Abstract

Due mainly to their unique antimicrobial property, silver nanoparticles (nAg) are used in everyday consumer products, such as cosmetics and textiles. It is expected that their use will only increase as the nanotechnology industry grows, resulting in a higher risk of nAg pollution in aquatic ecosystems and higher risk of uptake by fish. Previous studies have shown nAg to be harmful to fish, but little have focused on the cardiac impact these nanoparticles have. Callaghan et al. (2018) showed that nAg decreased cardiac contraction rate and peak contractile force in rainbow trout (Oncorhynchus mykiss) and suggested the nanoparticles induced these effects by impairing important proteins involved in excitation contraction coupling. This study aimed to investigate the mechanisms behind the nAg-induced cardiac contraction effects, determine if these effects were reversible and determine if cell size was influential. Ventricular strips from diploid Arctic char (Salvelinus alpinus) and diploid and triploid brook trout (Salvelinus fontinalis) were mounted in an isometrically contracting muscle physiology system to assess the effects of nAg as well as nifedipine and ryanodine on the force-frequency relationship, peak contractile force and post-rest potentiation (% PRP). nAg treatment of Arctic char strips resulted in a significantly higher mean maximum pacing frequency and lower mean peak force, suggesting nAg-interference with Na+/Ca2+ exchanger. Recovery tests involving the replenishment of saline were not successful, thereby implying nAg cardiac effects to be irreversible. No significant differences in peak force and % PRP of brook trout arose from nAg treatment, either pharmaceutical treatment or ploidy which suggested possible differences between species in excitation contraction coupling and nAg effects. Na+/K+ and total ATPase activity was also assessed in brook trout injected with 700 μg per kg nAg 24 hours before sampling and demonstrated nAg to decrease Na+/K+ ATPase activity significantly in both diploid and triploid fish, leading to the conclusion that nAg may affect cardiac contraction through at least two mechanisms: Na+/Ca2+ exchangers and Na+/K+ ATPases.