The mechanism of acute silver nitrate toxicity in freshwater rainbow trout (Oncorhynchus mykiss) is inhibition of gill Na⁺ and Cl^- transport

Rainbow trout (Oncorhynchus mykiss) were exposed to 2 and 10 μg l^-1 silver (as AgNO₃) for up to 75 h in moderately hard freshwater. At 10 μg l^-1 total Ag, branchial Na⁺ and Cl^- influxes were inhibited by over 50% immediately and by almost 100% at 8 h, and showed no signs of recovery over the duration of the experiment. Na⁺ and Cl^- effluxes were much less affected. These changes in unidirectional fluxes resulted in a large net loss of both Na⁺ and Cl^- across the gills and a significant decrease in plasma [Na⁺] and [Cl^-]. The effects of exposure to 2 μg l^-1 Ag on Na⁺ and Cl^- transport were generally similar to those at 10 μg l^-1, but were of a lesser magnitude. Unidirectional Na⁺ fluxes recovered immediately following removal of silver, after 48 h exposure to 2 μg l^-1. Michaelis-Menten kinetic analysis demonstrated that the maximal rate of Na⁺ influx (J(max)) was significantly reduced after 48 h exposure to 2 μg l^-1 Ag, whereas the affinity of the transport sites for Na⁺ (1/K(m)) was unaffected, indicating that the inhibition of Na⁺ influx by silver was of a non-competitive nature. Fish exposed to 10 μg l^-1 Ag for 48 h also had significantly lower activities of the branchial enzymes Na⁺/K⁺ ATPase (85% inhibition) and carbonic anhydrase (28% inhibition). The results of this study suggest that a disturbance of branchial ionoregulation, as a result of inhibition of branchial enzymes involved in ion transport, is the principal mechanism of the physiological toxicity of silver nitrate to freshwater fish.