Mechanism of acute silver toxicity in the euryhaline copepod Acartia tonsa

Acute silver effects on whole-body ion regulation and Na+,K+-ATPase activity were evaluated in the euryhaline copepod Acartia tonsa. Experiments were run at 20 °C, three different salinities (5, 15 and 30 ppt), in either the absence or the presence of food (diatom Thalassiosira weissflogii; 2 × 104 cells/mL). Standard static-renewal procedures were used. Copepods were acutely (48 h) exposed to silver (AgNO3) concentrations equivalent to the 48-h EC10 (dissolved Ag = 3, 49, and 94 μg/L), 48-h EC30 (dissolved Ag = 5, 71, and 125 μg/L) or 48-h EC50 (dissolved Ag = 7, 83, and 173 μg/L) values in the absence of food or to the 48-h EC50 (dissolved Ag = 35, 90, and 178 μg/L) values in the presence of food. These values were previously determined under the same experimental conditions at salinities 5, 15 and 30 ppt, respectively. Endpoints analyzed were whole-body ion concentrations (Na+, Cl−, and Mg2+) and Na+,K+-ATPase activity. In starved copepods, lower whole-body Na+ and Mg2+ concentrations were observed in salinities 5 and 30 ppt, respectively. Also a higher whole-body Na+,K+-ATPase activity was observed in all salinities tested. Data from fed copepods indicate that all these salinity effects were completely associated with starvation. Silver exposure induced a decrease in the whole-body Mg2+ concentration in starved copepods in salinities 5 and 30 ppt and a Na+,K+-ATPase inhibition in both starved and fed copepods in all salinities tested. Thus, food addition in the experimental media completely protected against silver effects on Mg2+ concentration, but not against those on Na+,K+-ATPase activity. In starved copepods, enzyme inhibition was dependent on silver concentration and a relationship between this parameter and mortality was observed in all salinities tested. Therefore, Na+,K+-ATPase molecules seem to be a key site for acute silver toxicity in marine invertebrates, as reported for freshwater fish and crustaceans.