In Vivo Action of Ammonia on Ion Transport Function in Liver and Heart Mitochondria of Immersion-Stressed Air-Breathing Fish (Anabas testudineus Bloch)

Ammonia, as an endogenous respiratory gas, is produced during protein and amino acid metabolism. Accumulation of excess ammonia is toxic, and fishes have developed mechanisms to defend against ammonia toxicity. Here, we tested the in vivo action of ammonia in an air-breathing fish to find how it modulates mitochondrial ion transport in fish heart and liver. We thus analysed the activity pattern of mitochondrial ion transporters such as mitochondrial Ca²⁺ATPase, mitochondrial H⁺ATPase and mitochondrial F₁F₀ ATPase in heart and liver of air-breathing fish Anabas testudineus which were kept for immersion-induced hypoxia stress. In addition, plasma metabolites such as glucose and lactate were also quantified. Oral administration of ammonia solution [(NH₄)₂SO₄; 50ng g^-1] for  30 min increased mit.Ca²⁺ATPase activity in heart but lowered its activity in liver mitochondria. A reduced mit.H⁺ATPase activity was found in heart but in liver its activity showed increase after ammonia treatment. F₁F₀ ATPase increased significantly in heart but showed reduced activity in liver mitochondria. Administration of ammonia in immersion-stressed fish, however, nullified the excitatory response of heart and liver mitochondria in the immersion-stressed fish. Overall, the data indicate that ammonia can play a significant physiological role in the regulation of mitochondrial ion homeostasis in the liver and heart of air-breathing fish during their acclimation to hypoxia stress.