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

Adult rainbow trout, fitted with arterial catheters, were exposed to AgNO3 for 6 days at a concentration (10 mu g 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+ in 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.