Abstract
Smolting Atlantic salmon, Salmo salar, were kept from 11 April to 24 May in soft water of pH 5 or in soft water of pH 5 and 50 μg aluminum (Al)∙L−1. Control fish were kept in soft water of pH 6.3–6.5. Water temperature was 8–14 °C. In mid-May, some of the control smolts were transferred to the test conditions for 8 d. Exposure to acid water resulted in osmoregulatory failure and high mortality rate. Al strongly enhanced toxicity. Sensitivity to low pH or low pH/Al exposure greatly increased when fish had developed to seawater tolerant smolts. In control and acid-exposed fish, gill carbonic anhydrase activity remained unchanged throughout the experiment whereas in Al-exposed fish, carbonic anhydrase activity decreased. Gill Na+K+-ATPase activity in control fish peaked in mid-May simulanteously with development of seawater tolerance. Fish from both acid-exposed groups had low seawater tolerance. Na+,K+-ATPase activity declined to 60% of start value in acid-exposed fish and to parr level in Al-exposed fish. Hypoosmoregulatory ability was linearly correlated with gill Na+K+-ATPase activity. Reduction in plasma Na+concentration in acid-exposed fish was linearly correlated with the reduction in gill Na+,K+-ATPase activity.
Published Version
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