The time course of silver accumulation in rainbow trout during static exposure to silver nitrate: Physiological regulation or an artifact of the exposure conditions?

Tammie P. Morgan, Martin Grosell, Richard C. Playle, Chris M. Wood

Research output: Contribution to journalArticle

26 Citations (Scopus)

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 (1-5g) were exposed in a static system to 110mAg labeled AgNO 3 at a total concentration of 1.92μg Agl-1 for 24h in synthetic soft water. Periodically throughout the exposure, gill and body 110mAg accumulation, gill and body 24Na 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 3h of exposure and then decreased until a plateau was reached at 12h of exposure. Body (minus gills) silver levels increased steadily over the exposure period until 18h of exposure. Whole body Na+ uptake decreased, was maximally inhibited by 3h of exposure but recovered by 12h despite continued silver exposure. Gill Na+K+-ATPase activity was not inhibited until 5h of exposure. The water dissolved silver concentration declined by ~70% over the 24h exposure period and the TOC content of the water increased over three-fold during the first 2h 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 2h of exposure. Apical silver uptake into the gills decreased over the initial 2.5h 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.

Original languageEnglish
Pages (from-to)55-72
Number of pages18
JournalAquatic Toxicology
Volume66
Issue number1
DOIs
StatePublished - Jan 7 2004

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physiological regulation
Silver Nitrate
silver nitrate
Oncorhynchus mykiss
Silver
silver
Artifacts
rainbow
artifact
nitrate
gills
sodium-potassium-exchanging ATPase
uptake mechanisms
Water
total organic carbon
Carbon
regulation
exposure
exposure duration
carbon

Keywords

  • Bioavailability
  • Biotic ligand model
  • Dissolved organic carbon
  • Na K-ATPase
  • Na uptake
  • Particulate organic carbon

ASJC Scopus subject areas

  • Aquatic Science

Cite this

The time course of silver accumulation in rainbow trout during static exposure to silver nitrate : Physiological regulation or an artifact of the exposure conditions? / Morgan, Tammie P.; Grosell, Martin; Playle, Richard C.; Wood, Chris M.

In: Aquatic Toxicology, Vol. 66, No. 1, 07.01.2004, p. 55-72.

Research output: Contribution to journalArticle

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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 (1-5g) were exposed in a static system to 110mAg labeled AgNO 3 at a total concentration of 1.92μg Agl-1 for 24h in synthetic soft water. Periodically throughout the exposure, gill and body 110mAg accumulation, gill and body 24Na 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 3h of exposure and then decreased until a plateau was reached at 12h of exposure. Body (minus gills) silver levels increased steadily over the exposure period until 18h of exposure. Whole body Na+ uptake decreased, was maximally inhibited by 3h of exposure but recovered by 12h despite continued silver exposure. Gill Na+K+-ATPase activity was not inhibited until 5h of exposure. The water dissolved silver concentration declined by ~70{\%} over the 24h exposure period and the TOC content of the water increased over three-fold during the first 2h 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 2h of exposure. Apical silver uptake into the gills decreased over the initial 2.5h 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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N2 - 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 (1-5g) were exposed in a static system to 110mAg labeled AgNO 3 at a total concentration of 1.92μg Agl-1 for 24h in synthetic soft water. Periodically throughout the exposure, gill and body 110mAg accumulation, gill and body 24Na 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 3h of exposure and then decreased until a plateau was reached at 12h of exposure. Body (minus gills) silver levels increased steadily over the exposure period until 18h of exposure. Whole body Na+ uptake decreased, was maximally inhibited by 3h of exposure but recovered by 12h despite continued silver exposure. Gill Na+K+-ATPase activity was not inhibited until 5h of exposure. The water dissolved silver concentration declined by ~70% over the 24h exposure period and the TOC content of the water increased over three-fold during the first 2h 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 2h of exposure. Apical silver uptake into the gills decreased over the initial 2.5h 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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