The physiological effects of waterborne silver exposure (added as AgNO3) on
spiny dogfish, Squalus acanthias, were evaluated at 30, 200 and 685 mug si
lver per I in 30 parts per thousand seawater. These concentrations cover th
e toxic range observed for freshwater teleosts, where silver is extremely t
oxic, to seawater teleosts which tolerate higher silver concentrations. How
ever, these levels are considerably higher than those that occur in the nor
mal environment. At 685 mug l(-1), dogfish died within 24 h. Causes of deat
h were respiratory as well as osmoregulatory failure. Arterial PaO2 rapidly
declined below 20 Tort, and blood acidosis (both respiratory and metabolic
) occurred. Urea excretion increased dramatically and plasma urea dropped f
rom 340 to 225 mM. There were pronounced increases in plasma Na+, Cl-, and
Mg2+, indicative of ionoregulatory failure due to increased diffusive perme
ability as well as inhibited NaCl excretion. At 200 mug l(-1), fish died be
tween 24 and 72 h of silver exposure. The same physiological events occurre
d with a small time delay. At 30 mug l(-1), effects were much less severe,
although slight mortality (12.5%) still occurred. Respiratory alkalosis occ
urred, together with moderate elevations in plasma Na+ and Cl- levels. Silv
er accumulated to the highest concentrations on gills, with only low levels
in the intestine, in accord with the virtual absence of drinking. Na+/K+-A
TP-ase activities of gill and rectal gland tissue were impaired at the high
est silver concentration. Normal gill function was impaired due to swelling
and fusion of lamellae, lamellar aneurism and lifting of the lamellar epit
helium. Our results clearly indicate that this elasmobranch is much more se
nsitive (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 th
e latter. (C) 2001 Elsevier Science B.V. All rights reserved.