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

Physiological effects of exposure to silver (AgClnn-1; 250 mu g Ag l(-1) or 1000 mu g Ag l(-1)) in seawater fish were investigated using adult starry flounders. While all fish survived up to 10 days in 250 mu g Ag l(-1), flou nders started to die after day 4 in 1000 mu g l(-1). Dose-dependent increas es in plasma and hepatic silver concentrations showed that silver was avail able for uptake. There were minimal negative effects on hematological param eters, acid-base status, and blood gases. Plasma ammonia showed a pronounce d (three- to four-fold), but transient increase in flounders exposed to eit her 250 mu g Ag l(-1) or 1000 mu g Ag l(-1). Whole body ammonia and acid eq uivalent efflux measurements indicated that ammonia retention was due to a combination of stimulated production and inhibited excretion. In the 1000-m u g Ag l(-1) group there was a similar transient increase in plasma [magnes ium], 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 mu g 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 wer e accompanied by a marked suppression of drinking, thereby indicating that acute silver toxicity was likely caused by a combination of elevated electr olyte concentrations and dehydration.