Abstract

The pattern of gill silver accumulation in rainbow trout during waterborne silver exposure has been reported to be unusual, reaching a peak in the first few hours of silver exposure followed by a marked decline with continued exposure. The potential causes of the pattern were investigated. Rainbow trout (1–5 g) were exposed in a static system to 110 m Ag labeled AgNO 3 at a total concentration of 1.92 μg Ag l −1 for 24 h in synthetic soft water. Periodically throughout the exposure, gill and body 110 m Ag accumulation, gill and body 24 Na uptake (from which whole body Na + uptake was calculated), gill Na +K +-ATPase activity, plus water silver (total and dissolved), Cl − and total organic carbon (TOC) concentrations were measured. Gill silver levels rapidly increased, peaked at 3 h of exposure and then decreased until a plateau was reached at 12 h of exposure. Body (minus gills) silver levels increased steadily over the exposure period until 18 h of exposure. Whole body Na + uptake decreased, was maximally inhibited by 3 h of exposure but recovered by 12 h despite continued silver exposure. Gill Na +K +-ATPase activity was not inhibited until 5 h of exposure. The water dissolved silver concentration declined by ∼70% over the 24 h exposure period and the TOC content of the water increased over three-fold during the first 2 h of exposure. There was a decrease in the calculated contribution of Ag + (from 20.9 to 2.5%) and an increase in the calculated contribution of Ag–TOC complexes (from 77 to 97.3%) to the total water silver concentration over the first 2 h of exposure. Apical silver uptake into the gills decreased over the initial 2.5 h of exposure while basolateral silver export out of the gills to the body remained constant throughout the exposure. The results of this study suggest that: (1) physiological regulation of silver movement may explain the pattern of gill silver accumulation observed in rainbow trout, although not by a mechanism coupled to Na +K +-ATPase inhibition as originally proposed; (2) alternatively or additionally, a decreased bioavailability of silver, due to the static exposure conditions, may explain the pattern of gill accumulation; (3) the early inhibition of whole body Na + uptake observed during silver exposure occurs via a mechanism other than Na +K +-ATPase inhibition; and (4) gill silver accumulation may be an appropriate endpoint for biotic ligand modeling.

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