The physiological responses of adult rainbow trout to a high level (30 000 μg l −1) of waterborne silver complexed by thiosulfate [Ag(S 2O 3) n −], as occurs in photoprocessing effluent, were compared with the responses to a low level of ionic Ag + (10 μg l −1 as AgNO 3). Ag(S 2O 3) n − was synthesized by combining one mole part AgCl with four mole parts of Na 2S 2O 3; responses to an equivalent level of Na 2S 2O 3 alone (1.11 mM) were examined as a control. Under flow-through conditions in moderately hard freshwater, 97% occurred as Ag(S 2O 3) 2 3−, 3% as AgS 2O 3 −, and a negligible fraction as ionic Ag + (< 0.003 μg l −1). Whereas 10 μg l −1 Ag (as AgNO 3) caused a variety of internal disturbances related to losses of plasma Na + and Cl −, 3000-fold greater Ag(S 2O 3) 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 Na 2S 2O 3 controls. Plasma Na +, Cl −, Ca 2+, K +, lactate, arterial blood P O 2 and P CO 2 , and hematology were essentially unaffected. Nevertheless, by Day 6, total gill Ag was 3-fold greater than during AgNO 3 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 AgNO 3 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.