The physiology of waterborne silver toxicity in freshwater rainbow trout (Oncorhynchus mykiss) 1. The effects of ionic Ag+

Chris M. Wood, McMaster University
Christer Hogstrand, McMaster University
Fernando Galvez, McMaster University
R. S. Munger, McMaster University

Abstract

Adult rainbow trout, fitted with arterial catheters, were exposed to AgNO3 for 6 days at a concentration (10 μg Ag l-1, flow-through) close to the 7 day LC50 in moderately hard freshwater. Approximately 35% of total Ag occurred as free ionic Ag+, and the remainder as silver chlorides. Ag accumulated on the gills and increased about 4-fold above control levels in blood plasma, stabilizing by 48 h. Much greater concentrations of Ag accumulated in the liver, but not the kidney, at 6 days. Metallothionein induction did not occur. Plasma [Na+] and [Cl-] declined steadily to 70% of control levels by day 6, accompanied by a progressive metabolic acidosis, a 5-fold increase in blood [glucose], a 40% decrease in relative plasma volume, contraction of the spleen, and marked hemoconcentration. Plasma [Ca2+] and [K+] were largely unaffected. Respiratory suffocation did not occur: plasma [lactate] remained constant, arterial P(O2), increased and P(CO2) decreased, the latter compensating the metabolic acidosis so arterial pH fell only moderately. Comparably sampled control fish exhibited negligible disturbance. Unidirectional Na+ influx from the water, measured in juvenile trout, was inhibited by 42% immediately, and abolished by 48 h of AgNO3 exposure. These symptoms suggested a similar toxic mechanism of action to that of low environmental pH. We speculate that Ag+ interferes with net Na+ and Cl- uptake at the gills, and causes death by secondary fluid volume disturbance, hemoconcentration, and eventual cardiovascular collapse.