LAUSR

Ammonia nitrogen exposure has been found to significantly increase the early apoptosis rates of gill cells, affect the contents of ATP and disturb expressions of calcium-related genes in clam Ruditapes philippinarum. Mitochondria are the centers for energy production, initiation of apoptosis and calcium signal regulation. It is hypothesized that gill mitochondrion is a target organelle for the ammonia nitrogen. Thus, ATP metabolism together with ATP-consuming functions would be interfered by ammonia exposure. In the present study, mitochondrial transmembrane potential (MTP), ATPase activities, gill functions in clearance and respiration, and histological changes were detected to characterize the effects of ammonia to the gill mitochondria in clam R. philippinarum. Results indicated that ammonia exposure led to significant decreases in MTP, Ca2+-ATPase activity and clearance rates. However, different concentrations of ammonia nitrogen induced different variations on H+, K+-ATPase activity and respiration rates. Histological observation revealed that subacute exposure of ammonia damaged the microstructure of gill tissues. Therefore, ammonia exposure dramatically damaged the normal structure and function of mitochondria, resulting in irreversible damage in energy formation and supply. In addition, it affected Ca2+ and K+ metabolism and inhibited food intake and respiration in clam R. philippinarum.