Mechanisms of PVP-functionalized silver nanoparticle toxicity in fish: Intravascular exposure disrupts cardiac pacemaker function and inhibits Na+/K+-ATPase activity in heart, but not gill

Abstract

Polyvinylpyrrolidone-functionalized silver nanoparticles (nAgPVP) are popular in consumer products for their colloidal stability and antimicrobial activity. Whole lake additions of nAgPVP cause long term, ecosystem-scale changes in fish populations but the mechanisms underlying this effect are unclear. We have previously shown that in fish, nAgPVP impairs cardiac contractility and Na+/K+-ATPase (NKA) activity in vitro, raising the possibility that heart dysfunction could underlie population-level exposure effects. The goal of this study was to determine if nAgPVP influences the control of heart rate (fh), blood pressure, or cardiac NKA activity in vivo. First, a dose-response curve for the effects of 5 nm nAgPVP on contractility was completed on isometrically contracting ventricular muscle preparations from Arctic char (Salvelinus alpinus) and showed that force production was lowest at 500 μg L−1 and maximum pacing frequency increased with nAgPVP concentration. Stroke volume, cardiac output, and power output were maintained in isolated working heart preparations from brook char (Salvelinus fontinalis) exposed to 700 μg L−1 nAgPVP. Both fh and blood pressure were elevated after 24 h in brook char injected with 700 μg kg body mass−1 nAgPVP and fh was insensitive to modulation with blockers of β-adrenergic and muscarinic cholinergic receptors. Na+/K+-ATPase activity was significantly lower in heart, but not gill of nAgPVP injected fish. The results indicate that nAgPVP influences cardiac function in vivo by disrupting regulation of the pacemaker and cardiomyocyte ionoregulation. Impaired fh regulation may prevent fish from appropriately responding to environmental or social stressors and affect their ability to survive.