Abstract The physiological effects of waterborne silver exposure (added as AgNO 3) on spiny dogfish, Squalus acanthias, were evaluated at 30, 200 and 685 μg silver per l in 30‰ seawater. These concentrations cover the toxic range observed for freshwater teleosts, where silver is extremely toxic, to seawater teleosts which tolerate higher silver concentrations. However, these levels are considerably higher than those that occur in the normal environment. At 685 μg l −1, dogfish died within 24 h. Causes of death were respiratory as well as osmoregulatory failure. Arterial P aO 2 rapidly declined below 20 Torr, and blood acidosis (both respiratory and metabolic) occurred. Urea excretion increased dramatically and plasma urea dropped from 340 to 225 mM. There were pronounced increases in plasma Na +, Cl −, and Mg 2+, indicative of ionoregulatory failure due to increased diffusive permeability as well as inhibited NaCl excretion. At 200 μg l −1, fish died between 24 and 72 h of silver exposure. The same physiological events occurred with a small time delay. At 30 μg l −1, effects were much less severe, although slight mortality (12.5%) still occurred. Respiratory alkalosis occurred, together with moderate elevations in plasma Na + and Cl − levels. Silver accumulated to the highest concentrations on gills, with only low levels in the intestine, in accord with the virtual absence of drinking. Na +/K +-ATP-ase activities of gill and rectal gland tissue were impaired at the highest silver concentration. Normal gill function was impaired due to swelling and fusion of lamellae, lamellar aneurism and lifting of the lamellar epithelium. Our results clearly indicate that this elasmobranch is much more sensitive (about 10-fold) to silver than marine teleosts, with silver's toxic action exerted on the gill rather than on the intestine, in contrast to the latter.