Abstract
In pristine natural waters, silver (Ag) occurs at low ngL -1 levels, rising to 1000-fold at highly contaminated sites. The free ion Ag + appears to be the sole cause of acute toxicity in freshwater, being among the most toxic of the metals in this regard, but probably does not occur to any significant extent in natural waters, where speciation is dominated by complexation to sulfide, dissolved organic carbon, chloride, and particles. Nevertheless, Ag + is the form used in regulatory tests, and on which environmental water quality criteria are based. Such criteria are often related to water hardness, but this probably reflects a misinterpretation of original test data, since other water quality parameters are far more protective than calcium and magnesium. The biotic ligand model approach holds promise for improving water quality criteria for Ag. In freshwater fish, waterborne Ag + poisons two key enzymes of ion transport in the gills (Na +/K +-ATPase and carbonic anhydrase), and death results from ionoregulatory failure. Dietborne toxicity is negligible. Silver appears to be taken up by sodium and copper transport pathways in the gills, as well as by diffusion of neutral complexes. Chronic toxicity occurs at much lower Ag concentrations, and may again involve ionoregulatory disturbance as well as other mechanisms. Acclimation may occur. In saltwater, Ag speciation is dominated by salinity-dependent chloride complexation, and Ag is far less toxic on an acute basis than in freshwater. Since seawater fish drink the medium, both gills and gut are targets of acute toxicity and potential routes of Ag uptake, but mechanisms remain unclear. Marine elasmobranchs are far more sensitive, and take up much more Ag, than marine teleosts. Bioconcentration of Ag clearly occurs in both freshwater and saltwater fish, but the bioconcentration factor approach is not a useful regulatory tool for Ag. Silver accumulates preferentially in the liver, which serves as a scavenging organ. Silver is a powerful inducer of metallothionein synthesis for detoxification. Biological half-lives are long and excretory mechanisms remain poorly characterized. Trophic transfer efficiency is low and biomagnification of Ag does not occur.
| Original language | English |
|---|---|
| Publisher | Unknown Publisher |
| Number of pages | 65 |
| Volume | 31 |
| Edition | PART B |
| DOIs | |
| State | Published - Jul 11 2011 |
Publication series
| Name | Fish Physiology |
|---|---|
| No. | PART B |
| Volume | 31 |
| ISSN (Print) | 15465098 |
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ASJC Scopus subject areas
- Animal Science and Zoology
- Physiology
Cite this
Silver. / Wood, Chris M.
PART B ed. Unknown Publisher, 2011. 65 p. (Fish Physiology; Vol. 31, No. PART B).Research output: Book/Report › Book
}
TY - BOOK
T1 - Silver
AU - Wood, Chris M.
PY - 2011/7/11
Y1 - 2011/7/11
N2 - In pristine natural waters, silver (Ag) occurs at low ngL -1 levels, rising to 1000-fold at highly contaminated sites. The free ion Ag + appears to be the sole cause of acute toxicity in freshwater, being among the most toxic of the metals in this regard, but probably does not occur to any significant extent in natural waters, where speciation is dominated by complexation to sulfide, dissolved organic carbon, chloride, and particles. Nevertheless, Ag + is the form used in regulatory tests, and on which environmental water quality criteria are based. Such criteria are often related to water hardness, but this probably reflects a misinterpretation of original test data, since other water quality parameters are far more protective than calcium and magnesium. The biotic ligand model approach holds promise for improving water quality criteria for Ag. In freshwater fish, waterborne Ag + poisons two key enzymes of ion transport in the gills (Na +/K +-ATPase and carbonic anhydrase), and death results from ionoregulatory failure. Dietborne toxicity is negligible. Silver appears to be taken up by sodium and copper transport pathways in the gills, as well as by diffusion of neutral complexes. Chronic toxicity occurs at much lower Ag concentrations, and may again involve ionoregulatory disturbance as well as other mechanisms. Acclimation may occur. In saltwater, Ag speciation is dominated by salinity-dependent chloride complexation, and Ag is far less toxic on an acute basis than in freshwater. Since seawater fish drink the medium, both gills and gut are targets of acute toxicity and potential routes of Ag uptake, but mechanisms remain unclear. Marine elasmobranchs are far more sensitive, and take up much more Ag, than marine teleosts. Bioconcentration of Ag clearly occurs in both freshwater and saltwater fish, but the bioconcentration factor approach is not a useful regulatory tool for Ag. Silver accumulates preferentially in the liver, which serves as a scavenging organ. Silver is a powerful inducer of metallothionein synthesis for detoxification. Biological half-lives are long and excretory mechanisms remain poorly characterized. Trophic transfer efficiency is low and biomagnification of Ag does not occur.
AB - In pristine natural waters, silver (Ag) occurs at low ngL -1 levels, rising to 1000-fold at highly contaminated sites. The free ion Ag + appears to be the sole cause of acute toxicity in freshwater, being among the most toxic of the metals in this regard, but probably does not occur to any significant extent in natural waters, where speciation is dominated by complexation to sulfide, dissolved organic carbon, chloride, and particles. Nevertheless, Ag + is the form used in regulatory tests, and on which environmental water quality criteria are based. Such criteria are often related to water hardness, but this probably reflects a misinterpretation of original test data, since other water quality parameters are far more protective than calcium and magnesium. The biotic ligand model approach holds promise for improving water quality criteria for Ag. In freshwater fish, waterborne Ag + poisons two key enzymes of ion transport in the gills (Na +/K +-ATPase and carbonic anhydrase), and death results from ionoregulatory failure. Dietborne toxicity is negligible. Silver appears to be taken up by sodium and copper transport pathways in the gills, as well as by diffusion of neutral complexes. Chronic toxicity occurs at much lower Ag concentrations, and may again involve ionoregulatory disturbance as well as other mechanisms. Acclimation may occur. In saltwater, Ag speciation is dominated by salinity-dependent chloride complexation, and Ag is far less toxic on an acute basis than in freshwater. Since seawater fish drink the medium, both gills and gut are targets of acute toxicity and potential routes of Ag uptake, but mechanisms remain unclear. Marine elasmobranchs are far more sensitive, and take up much more Ag, than marine teleosts. Bioconcentration of Ag clearly occurs in both freshwater and saltwater fish, but the bioconcentration factor approach is not a useful regulatory tool for Ag. Silver accumulates preferentially in the liver, which serves as a scavenging organ. Silver is a powerful inducer of metallothionein synthesis for detoxification. Biological half-lives are long and excretory mechanisms remain poorly characterized. Trophic transfer efficiency is low and biomagnification of Ag does not occur.
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U2 - 10.1016/S1546-5098(11)31001-1
DO - 10.1016/S1546-5098(11)31001-1
M3 - Book
VL - 31
T3 - Fish Physiology
BT - Silver
PB - Unknown Publisher
ER -