SUMMARY
At a field site in Belize, mangrove killifish Rivulus marmoratus inhabit hypersaline waters (up to 48 ‰) containing approximately 1 mmol l–1 ammonia. We tested the hypotheses that R. marmoratus modify their nitrogen metabolism and excretion (i) by accumulating free amino acids (FAAs) and urea in the tissues during hyperosmotic stress and (ii) by shifting to ureotelism and accumulating FAAs during hyperammonia stress. Urea excretion (JUrea) (but not ammonia excretion, JAmm) displayed a diurnal pattern, with significantly less (75 %) urea excreted at night than during the day in both laboratory-reared clones and wild-caught killifish. When fish were exposed to hypersaline conditions (45 ‰ sea water), JUrea was significantly reduced and tissue urea and FAA levels were elevated compared with those of control fish (15 ‰ sea water). When R. marmoratus were exposed to 0, 1, 2, 5 and 10 mmol l–1 NH4Cl (pH 8) for 48 h, no differences were found in JUrea. Remarkably, prolonged exposure (10 days) to 5 mmol l–1 NH4Cl (pH 8) did not result in an elevation of tissue ammonia levels. In addition, tissue urea and total FAA levels did not differ between control and ammonia-exposed fish after ⩾4 days. We propose that the euryhaline R. marmoratus retain urea and FAAs within their tissues in response to extreme osmotic stress. In contrast to many ammonia-tolerant fishes, R. marmoratus do not shift to ureotelism during prolonged hyperammonia stress, nor do they convert nitrogenous wastes into FAAs. The data suggest that killifish continue to eliminate ammonia despite an unfavourable blood-to-water gradient, thereby avoiding accumulation of ammonia.
Rapid increase in the partial pressure of NH3 on the cutaneous surface of air-exposed mangrove killifish, Rivulus marmoratus
