The effects of exposure to ammonia on ammonia and taurine pools of the symbiotic clam Solemya reidi

The nutrition of the gutless clam Solemya reidi is supported by the activity of intracellular chemoautotrophic bacteria housed in its gill filaments. Ammonia (the sum of NH3 and NH4+) is utilized as a nitrogen source by the association and is abundant in the clam’s environment. In the present study, clams were exposed to 0.01–1.3 mmol l−1 ammonia for 22–23 h in the presence of thiosulfate as a sulfur substrate. Ammonia exposure increased the ammonia concentration in the tissue pools of the gill, foot and visceral mass from 0.5 to 2 μmol g−1 wet mass, without added ammonia, to as much as 12 μmol g−1 wet mass in the presence of 0.7 and 1.3 mmol l−1 external ammonia. Gill tissue ammonia concentrations were consistently higher than those in the foot and visceral mass. The elevation of tissue ammonia concentration compared with the medium may be due in part to an ammonia trapping mechanism resulting from a lower intracellular pH compared with sea water and greater permeability to NH3 compared with NH4+. Rates of ammonia incorporation into organic matter (assimilation) were determined using 15N as a tracer. 15N-labeled ammonia assimilation was higher in gill than in foot and increased as a function of 15N-labeled ammonia concentration in the medium. The size of the free amino acid (FAA) pool in the gill also increased as a function of ammonia concentration in the medium. This entire increase was accounted for by a single amino acid, taurine, which was the predominant FAA in both gill and foot tissue. Aspartate, glutamate, arginine and alanine were also abundant but their levels were not influenced by external ammonia concentration. Ammonia assimilation appeared to occur at rates sufficient to account for the observed increase in taurine level. These findings suggest that taurine is a major product of ammonia assimilation.