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

Ian J. Morgan, Raymond P. Henry, Chris M. Wood

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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.

Original languageEnglish (US)
Pages (from-to)145-163
Number of pages19
JournalAquatic Toxicology
Issue number1-3
StatePublished - May 1997


  • Na and Cl transport
  • Oncorhynchus mykiss
  • Osmoregulation
  • Physiological toxicity
  • Rainbow trout
  • Silver nitrate

ASJC Scopus subject areas

  • Aquatic Science


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