The physiology of waterborne silver toxicity in freshwater rainbow trout (Oncorhynchus mykiss). 2. The effects of silver thiosulfate

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The physiological responses of adult rainbow trout to a high level (30,000 μg l-1) of waterborne silver complexed by thiosulfate [Ag(S2O3)(n)-] as occurs in photoprocessing effluent, were compared with the responses to a low level of ionic Ag+ (10 μg l-1 as AgNO3). Ag(S2O3)(n)- was synthesized by combining one mole part AgCl with four mole parts of Na2S2O3; responses to an equivalent level of Na2S2O3 alone (1.11 mM) were examined as a control. Under flow-through conditions in moderately hard freshwater, 97% occurred as Ag(S2O3)23-, 3% as AgS2O3-, and a negligible fraction as ionic Ag+ (< 0.003 μg l-1). Whereas 10 μg l-1 Ag (as AgNO3) caused a variety of internal disturbances related to losses of plasma Na+ and Cl-, 3000-fold greater Ag(S2O3)(n)- had very minor effects - a moderate, transient metabolic alkalosis and an apparent expansion of plasma volume. Plasma glucose declined slightly, but this also occurred in Na2S2O3 controls. Plasma Na+, Cl-, Ca2+, K+, lactate, arterial blood P(O2), and P(CO2), and hematology were essentially unaffected. Nevertheless, by Day 6, total gill Ag was 3-fold greater than during AgNO3 exposure, while plasma Ag was 3-4 times greater (stabilized by Day 2). There was also two-fold greater Ag accumulation in the liver than during AgNO3 exposure, as well as accumulation in kidney, and an induction of metallothionein in liver, gills, and kidney. We conclude that acute toxic effects of waterborne silver are caused by ionic Ag+ interacting with key functions at the gill surface and not by internal Ag accumulation. Even very high levels of waterborne silver are relatively benign when complexed by thiosulfate.

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Aquatic Toxicology

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