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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, T.P.; Grosell, M.; Playle, R.C.; Wood, C.M. (2004). The time course of silver accumulation in rainbow trout during static exposure to silver nitrate: physiological regulation or an artifact of the exposure conditions? Aquat. Toxicol. 66(1): 55-72. http://dx.doi.org/10.1016/j.aquatox.2003.07.003
In: Aquatic Toxicology. Elsevier Science: Tokyo; New York; London; Amsterdam. ISSN 0166-445X; e-ISSN 1879-1514
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| Trefwoorden |
Chemical elements > Metals > Alkali metals > Sodium
Models
Organic matter > Carbon > Organic carbon > Dissolved organic matter > Dissolved organic carbon
Organic matter > Particulates > Particulate organic matter > Organic carbon > Particulate organic carbon
Marien/Kust |
| Author keywords |
bioavailability; biotic ligand model; Na+ uptake; Na+K+-ATPase;dissolved organic carbon; particulate organic carbon |
| Auteurs | | Top |
- Morgan, T.P., correspondent
- Grosell, M.
- Playle, R.C.
- Wood, C.M.
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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 (1-5 g) were exposed in a static system to 110mAg labeled AgNO3 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 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 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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