Juvenile big bellied seahorse Hippocampus abdominalis were exposed acutely and chronically to elevated ammonia and nitrite {24 h exposure: 0·01, 5·0, 10·1, 14·8 and 19·9 mg l−1 total ammonia‐nitrogen [TA‐N] and <0·001, 74·4, 99·2 and 123·6 mg l−1 [NO2‐N] nitrite‐nitrogen and 35 days exposure: 0·11, 0·55, 1·67 and 3·07 mg l−1 TAN and <0·001, 0·92, 4·67 and 9·10 mg NO2‐N l−1}. Significant (P<0·001) increases in oxygen consumption rate and ventilation frequency occurred at 14·8, 19·9 mg l−1 TA‐N and 99·2, 123·6 mg l−1 NO2‐N for acutely exposed fish. Oxygen consumption rate was significantly (P<0·05) elevated at 1·67 and 3·07 mg l−1 TA‐N in chronically treated fish and ventilation frequency increased significantly (P<0·05) at 0·55, 1·67, 3·07 mg l−1 TA‐N and 4·59, 9·10 mg l−1 NO2‐N. There were no significant differences in growth between controls and ammonia exposed fish. Mortalities occurred at 14·8, 19·9 mg l−1 TA‐N.
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Adams et al. (2001) studied this question.
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