TY - JOUR
T1 - Water chloride provides partial protection during chronic exposure to waterborne silver in rainbow trout (Oncorhynchus mykiss) embryos and larvae
AU - Brauner, Colin J.
AU - Wilson, Jonathan
AU - Kamunde, Collins
AU - Wood, Chris M.
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2003/11
Y1 - 2003/11
N2 - Rainbow trout embryos and larvae were continuously exposed (at 12.5°C) to waterborne silver in a flow-through setup, from fertilization to swim-up, at nominal silver concentrations of 0, 0.1, or 1.0 μg/L total silver (as AgNO3) at three different water Cl- levels (30, 300, and 3,000 μM, added as KCl). Exposures were conducted in synthetic soft water (hardness 20 mg CaCO3/L generated from reconstituted reverse osmosis freshwater). Continuous exposure to 1.0 μg/L total silver for 58 d at 30 μM water Cl- resulted in a pronounced ionoregulatory disturbance (as indicated by a reduction in whole body Na+,K+-ATPase activity, unidirectional Na+ uptake [Jin Na+], and whole body Na+ and Cl- levels) and a reduction in extractable protein and wet weight. Thus, the mechanism of chronic silver toxicity appears to be similar to that observed during acute silver exposure in juvenile and adult fish, specifically an ionoregulatory disturbance. Higher water Cl- levels (300 and 3,000 μM Cl-) offered some degree of protection from the ionoregulatory disturbance, with only minor protective effects in terms of mortality. The protective effects of water Cl- on the toxicity of silver (as AgNO3) appear to be far less during chronic than during acute exposure. Mortality and larval Na + concentration, Jin Na+, and Na +,K+-ATPase activity all appear to be correlated with silver body burden and calculated water Ag+ during chronic silver exposure. Thus, there appears to be potential to model chronic toxicity but not simply by recalibration of an acute model. A chronic model must be based on real chronic data because the protective effects of various ligands appear to be quantitatively very different from those in the acute situation.
AB - Rainbow trout embryos and larvae were continuously exposed (at 12.5°C) to waterborne silver in a flow-through setup, from fertilization to swim-up, at nominal silver concentrations of 0, 0.1, or 1.0 μg/L total silver (as AgNO3) at three different water Cl- levels (30, 300, and 3,000 μM, added as KCl). Exposures were conducted in synthetic soft water (hardness 20 mg CaCO3/L generated from reconstituted reverse osmosis freshwater). Continuous exposure to 1.0 μg/L total silver for 58 d at 30 μM water Cl- resulted in a pronounced ionoregulatory disturbance (as indicated by a reduction in whole body Na+,K+-ATPase activity, unidirectional Na+ uptake [Jin Na+], and whole body Na+ and Cl- levels) and a reduction in extractable protein and wet weight. Thus, the mechanism of chronic silver toxicity appears to be similar to that observed during acute silver exposure in juvenile and adult fish, specifically an ionoregulatory disturbance. Higher water Cl- levels (300 and 3,000 μM Cl-) offered some degree of protection from the ionoregulatory disturbance, with only minor protective effects in terms of mortality. The protective effects of water Cl- on the toxicity of silver (as AgNO3) appear to be far less during chronic than during acute exposure. Mortality and larval Na + concentration, Jin Na+, and Na +,K+-ATPase activity all appear to be correlated with silver body burden and calculated water Ag+ during chronic silver exposure. Thus, there appears to be potential to model chronic toxicity but not simply by recalibration of an acute model. A chronic model must be based on real chronic data because the protective effects of various ligands appear to be quantitatively very different from those in the acute situation.
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U2 - 10.1086/378136
DO - 10.1086/378136
M3 - Article
C2 - 14988795
AN - SCOPUS:2142668180
VL - 76
SP - 803
EP - 815
JO - Physiological and Biochemical Zoology
JF - Physiological and Biochemical Zoology
SN - 1522-2152
IS - 6
ER -