Physiology of acute silver toxicity in the starry flounder (Platichthys stellatus) in seawater

C. Hogstrand, University of Kentucky
E. A. Ferguson, University of Kentucky
J. R. Shaw, University of Kentucky
F. Galvez, McMaster University
N. A. Webb, McMaster University
C. M. Wood, McMaster University


Physiological effects of exposure to silver (AgCl(n)(n)-1; 250 μg Ag l-1 or 1000 μg Ag l-1) in seawater fish were investigated using adult starry flounders. While all fish survived up to 10 days in 250 μg Ag l-1, flounders started to die after day 4 in 1000 μg 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 μg Ag l-1 or 1000 μg 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 1000μg 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 μg 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.