Physiology and modeling of mechanisms of silver uptake and toxicity in fish

Abstract

In this review, we outline the physiological and toxicological effects of silver (Ag) in freshwater and marine fish. For freshwater fish, the acute toxicity of Ag appears to be caused solely by ionic Ag + interacting at the gills, inhibiting basolateral Na + , K + ‐ATPase activity. Disruption of this enzyme inhibits active Na + and Cl − uptake and therefore osmoregulation by the fish. Silver is much less toxic to marine fish, mainly because ionic Ag + is complexed by Cl − , but the mechanisms of acute toxicity and the toxic species of Ag are poorly understood. Osmoregulatory failure occurs in marine fish exposed to high concentrations of Ag, and the intestine appears to be a primary toxic site of action, perhaps along with a gill component. Modeling approaches to calculate Ag interactions at biological surfaces are used to illustrate the effects of water chemistry on Ag speciation and therefore toxicity to freshwater and marine fish. In these models, the most important components affecting Ag speciation are the complexing agents Cl − and dissolved organic matter followed by the competing agents Na + and Ca 2+ , although a particulate component may be important to incorporate into the models in future. More precise knowledge of the actual toxic sites of Ag is necessary if we are to fully understand the effects of waterborne Ag in the environment.