Physiological effects of exposure to silver (AgClnn-1; 250 micrograms Ag l-1 or 1000 micrograms Ag l-1) in seawater fish were investigated using adult starry flounders. While all fish survived up to 10 days in 250 micrograms Ag l-1, flounders started to die after day 4 in 1000 micrograms l-1. Dose-dependent increases in plasma and hepatic silver concentrations showed that silver was available for uptake. There were minimal negative effects on hematological parameters, acid-base status, and blood gases. Plasma ammonia showed a pronounced (three- to four-fold), but transient increase in flounders exposed to either 250 micrograms Ag l-1 or 1000 micrograms Ag l-1. Whole body ammonia and acid equivalent efflux measurements indicated that ammonia retention was due to a combination of stimulated production and inhibited excretion. In the 1000-microgram Ag l-1 group there was a similar transient increase in plasma [magnesium], which was restored by day 4. In contrast, plasma chloride and sodium levels increased gradually towards the point when fish began to die. At 250 micrograms Ag l-1, the Na+/K(+)-ATPase activity of the intestine was unaffected but there was a two-fold increase in branchial Na+/K(+)-ATPase activity. The latter effect was interpreted as compensation for an elevated chloride and sodium load. The increases in plasma chloride and sodium concentrations were accompanied by a marked suppression of drinking, thereby indicating that acute silver toxicity was likely caused by a combination of elevated electrolyte concentrations and dehydration.