Exposure to elevated silver (as AgNO 3) concentrations (6–9 μM) in seawater was associated with comparably high silver concentrations in the intestinal fluids of the lemon sole ( Parophrys vetulus), and a tendency for reduced drinking rate. The effects of silver on intestinal ion and acid-base regulation were studied using in situ perfusion of the intestine. Intestinal net Cl − uptake was reduced from 0.4 to 0.1 and intestinal net Na + uptake from 0.2 to 0 mmol kg −1 h −1 during silver exposure (9 μM). At the same time, intestinal HCO 3 − net efflux was reduced from 0.2 to 0.1 mmol kg −1 h −1. Both intestinal Na + and Cl − uptake and Cl −/HCO 3 − exchange are thus sensitive to silver, but to different extents. None of the observed effects were reversible during 24 h of recovery. Intestinal water transport was highly variable in vivo in the perfused preparation, and no significant effect of silver exposure was observed. However, in vitro intestine preparations exhibited reduction of intestinal net water flux from 4 to 1 μl cm −2 h −1 during silver exposure together with reduced unidirectional Cl − influx. Reduced water intake and transepithelial water transport in silver-exposed fish resulted in moderate hemoconcentration evident from higher hematocrit values, but not in increased plasma ion levels. The latter could reflect a compensatory response via increased branchial Na +/K +-ATPase levels, observed in silver-exposed fish, indicative of increased branchial ion transport capacity. Impairment of intestinal ion and water transport as a result of silver intake via drinking could be an important part of the fatal cascade of physiological effects observed in marine fish during acute silver exposure.