Ionoregulatory development and the effect of chronic silver exposure on growth, survival, and sublethal indicators of toxicity in early life stages of rainbow trout (Oncorhynchus mykiss).

Rainbow trout embryos and larvae were continuously exposed, in a flow-through system, to 0, 0.1 microg/l (measured=0.098 +/- 0.002 microg/l) or 1.0 microg/l (measured=0.853+/-0.022 microg/l) total silver (as AgNO3) in moderately hard water (120 mg CaCO3/l, 0.70 mM Cl, 1.3 mg/l dissolved organic matter and 13.7 +/- 0.1 degrees C) from fertilization to I week post-hatch. The objectives of the study were to investigate the effects of chronic silver exposure on mortality, time to hatch and growth, and on sublethal physiological indicators of toxicity. Exposure to 1.0 microg/l total silver resulted in a small, but statistically significant, increase in mortality (16%) relative to controls (12%) but interestingly, resulted in an increased rate of growth (as indicated by larval weight, length and extractable protein) and ionoregulatory development over the duration of this study. Whole body unidirectional Na uptake (J(in)Na+) increased with silver exposure concentration (both 0.1 microg/l and 1.0 microg/l total silver) just prior to and following hatch, with up to a three-fold elevation in J(in)Na+ in the 1.0 microg/l treatment relative to controls. Qualitatively similar changes in whole body Na+,K-ATPase activity (per mg protein or per whole embryo or larvae) also occurred over this period. By 1 week post-hatch, there were no differences in J(in)Na among treatments and Na+,K+-ATPase activity levels in silver exposed groups were significantly reduced relative to controls. Within 2 days following hatch, there was an elevation in whole larval ammonia levels, while cortisol levels were elevated at 1 week post-hatch in the 1.0 microg/l treatment relative to controls. Ionoregulatory disturbance and elevations in both cortisol and ammonia have also been observed during acute silver exposure in adult rainbow trout, indicating that chronic and acute mechanisms of toxicity may be similar.