Physiological analysis of the stress response associated with acute silver nitrate exposure in freshwater rainbow trout (Oncorhynchus mykiss)

Abstract

AbstractRainbow trout were exposed to AgNO3 (9.2 μg/L total Ag, of which 35% was as the free ion, Ag+) for a 6‐d period in dechlorinated Hamilton tapwater. Our findings suggest that the primary toxic mechanism of Ag is an interruption of ionoregulation at the gills, stopping active Na+ and Cl− uptake without increasing passive efflux, thereby causing net ion loss. There is no recovery of influxes over 6 d, whereas effluxes are gradually reduced below control levels, and ion balance remains negative. The resulting fall in plasma [Na+] and [Cl−] leads to a decrease in plasma volume and hemoconcentration, but the red blood cells do not swell. A substantial metabolic acidosis with partial respiratory compensation occurs in the blood, due to a net uptake of acidic equivalents from the environmental water. This uptake greatly exceeds the measured acid load in the extracellular fluid, suggesting that acidosis also occurs in the intracellular compartment, which in turn explains the continual loss of K+ to the water in the absence of any change in plasma [K+]. Plasma ammonia, glucose, and cortisol rise. As there is no reduction but rather a progressive rise in ammonia excretion, the increase in plasma ammonia is due to elevated metabolic production rather than inhibited excretion. The cause is probably the stress‐induced mobilization of cortisol. This increased plasma ammonia, in conjunction with hyperventilation, helps to counteract metabolic acidosis. However, because the fish is unable to counteract the loss of plasma ions, death eventually results from a severe ionoregulatory disturbance.