Zinc oxide nanoparticles trigger cardiorespiratory stress and reduce aerobic scope in the white sucker, Catostomus commersonii

Abstract

Acute exposure to commercially-relevant zinc oxide nanoparticles (nZnO) can alter heart function and induce a cellular stress response in gill tissue of the white sucker (Catostomus commersonii), a freshwater teleost fish. The current study aimed to identify potential mechanisms underlying the cardiorespiratory effects of nZnO exposure and to characterize the ecophysiological importance of nZnO toxicity. Gill morphology in white suckers exposed to nZnO was examined by scanning electron microscopy and indications of mild irritation were observed. Cardiorespiratory function was assessed using electrocardiography and opercular pressure fluctuations and the caudal artery was cannulated for injection of the acetylcholine receptor antagonist atropine to eliminate vagal influence on the heart. Exposure to nZnO had no significant effect on heart rate under the conditions tested, but ventilation rate rose ~30% in treated fish. Administration of atropine increased ventilation rate by 55% in control fish but had no effect in treated animals, indicating that nZnO alters parasympathetic control of respiration. Heart acetylcholinesterase activity decreased in nZnO-exposed fish, implying impaired acetylcholine metabolism may contribute to cardiorespiratory toxicity. Exposure to nZnO did not activate anaerobic metabolism, as we observed no changes in muscle lactate dehydrogenase kinetics or pH sensitivity. Decreases in both the maximum rate of oxygen consumption and aerobic scope indicate that exposure to nZnO reduces the aerobic capacity of the animal and suggests the observed toxicity has potential ecological importance. Overall, our findings suggest that nZnO-mediated damage to the gill epithelium alters cardiorespiratory regulation and subsequently impairs oxygen uptake and delivery.