Abstract
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 language | English |
|---|---|
| Pages (from-to) | 145-163 |
| Number of pages | 19 |
| Journal | Aquatic Toxicology |
| Volume | 38 |
| Issue number | 1-3 |
| DOIs | |
| State | Published - May 1 1997 |
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Keywords
- Na and Cl transport
- Oncorhynchus mykiss
- Osmoregulation
- Physiological toxicity
- Rainbow trout
- Silver nitrate
ASJC Scopus subject areas
- Aquatic Science
Cite this
The mechanism of acute silver nitrate toxicity in freshwater rainbow trout (Oncorhynchus mykiss) is inhibition of gill Na+ and Cl- transport. / Morgan, Ian J.; Henry, Raymond P.; Wood, Chris M.
In: Aquatic Toxicology, Vol. 38, No. 1-3, 01.05.1997, p. 145-163.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The mechanism of acute silver nitrate toxicity in freshwater rainbow trout (Oncorhynchus mykiss) is inhibition of gill Na+ and Cl- transport
AU - Morgan, Ian J.
AU - Henry, Raymond P.
AU - Wood, Chris M.
PY - 1997/5/1
Y1 - 1997/5/1
N2 - 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.
AB - 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.
KW - Na and Cl transport
KW - Oncorhynchus mykiss
KW - Osmoregulation
KW - Physiological toxicity
KW - Rainbow trout
KW - Silver nitrate
UR - http://www.scopus.com/inward/record.url?scp=0030958691&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030958691&partnerID=8YFLogxK
U2 - 10.1016/S0166-445X(96)00835-1
DO - 10.1016/S0166-445X(96)00835-1
M3 - Article
AN - SCOPUS:0030958691
VL - 38
SP - 145
EP - 163
JO - Aquatic Toxicology
JF - Aquatic Toxicology
SN - 0166-445X
IS - 1-3
ER -