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Thyroid hormone metabolite 3, 5-diiodothyronine (T2) has been shown to possess physiological actions in vertebrates including fishes. It is, however, not certain if T2 has a role in cation transport in fish hepatocytes, particularly in a stressed condition. We, therefore, tested the in vitro action of T2 on the activities of ion transporters such as Na+/K+ ATPase, H+/ K+ ATPase, Na+/NH4 + ATPase, vacuolar H+-ATPase, Plasma Membrane Ca2+ ATPase (PMCA), mitochondrial Ca2+ and mitochondrial H+-ATPase as these ATPases are known for their roles in maintaining systemic and cellular cation gradients including proton and potassium gradients. Hepatocyte explants of air-breathing fish (Anabas testudineus, Bloch), either in non-stressed or hypoxic condition, were incubated with varied doses of T2 (10-9, 10-8 and 10-7 M) for 15 min and the specific activities of these cation-dependent ATPases were analyzed. We found that T2 exposure evoked higher sensitivity to vacuolar and mitochondrial H+-ATPases and H+/K+ ATPase and not to PMCA or mitochondrial Ca2+ ATPase. The data also indicated that T2 has a similar sensitivity to vacuolar and mitochondrial H+-ATPases and H+/K+ ATPase in the hepatocytes of both non-stressed and hypoxia-stressed fish. The data thus provide evidence for a direct action of T2 on the regulation of proton and potassium gradients in the hepatocytes of both non-stressed and hypoxicair-breathing fish.

Thyroid hormone metabolite 3, 5-diiodothyronine (T2) has been shown to possess physiological actions in vertebrates including fishes. It is, however, not certain if T2 has a role in cation transport in fish hepatocytes, particularly in a stressed condition. We, therefore, tested the in vitro action of T2 on the activities of ion transporters such as Na+/K+ ATPase, H+/ K+ ATPase, Na+/NH4 + ATPase, vacuolar H+-ATPase, Plasma Membrane Ca2+ ATPase (PMCA), mitochondrial Ca2+ and mitochondrial H+-ATPase as these ATPases are known for their roles in maintaining systemic and cellular cation gradients including proton and potassium gradients. Hepatocyte explants of air-breathing fish (Anabas testudineus, Bloch), either in non-stressed or hypoxic condition, were incubated with varied doses of T2 (10-9, 10-8 and 10-7 M) for 15 min and the specific activities of these cation-dependent ATPases were analyzed. We found that T2 exposure evoked higher sensitivity to vacuolar and mitochondrial H+-ATPases and H+/K+ ATPase and not to PMCA or mitochondrial Ca2+ ATPase. The data also indicated that T2 has a similar sensitivity to vacuolar and mitochondrial H+-ATPases and H+/K+ ATPase in the hepatocytes of both non-stressed and hypoxia-stressed fish. The data thus provide evidence for a direct action of T2 on the regulation of proton and potassium gradients in the hepatocytes of both non-stressed and hypoxicair-breathing fish.

The neuronal circuitries of brain and the corresponding ion transporters contribute to the maintenance of ion homeostasis in fish brain. The sensitivity of these neuronal clusters in response to environmental clues brings neural plasticity and subsequent regulation of stress acclimation. Nitric oxide (NO), a gasotransmitter, is involved in ion transport in many peripheral tissues of fishes including air-breathing fish. However, the role of NO in mitochondrial ion transporter activity has not yet been investigated in fish brain. We, therefore, investigated the short-term in vivo action of a NO donor, Sodium Nitro-Prusside (SNP), on mitochondrial ion transporters such as H+- Ca2+- and Mg2+-dependent ATPases in brain segments such as Prosen-Cephalon (PC), Mesen-Cephalon (MC) and Meten-Cephalon (MeC) of immersion-stressed Anabas testudineus. Intraperitoneal injection of SNP for 30 min lowered the activities of bafilomycin-sensitive H+ATPase and vanadate sensitive Ca2+ATPase in PC, whereas in MeC, these transporters showed significant rise in activities after SNP treatment. The oligomycin-sensitive Mg2+ATPase activity showed a significant decrease in PC and MC of brain after SNP treatment in non-stressed fish. Induction of stress by water immersion altered the activities of these ion transporter activities. However, the treatment of SNP in immersed fish showed recovery of the immersion-induced modulation in the activities of these mitochondrial ion transporters. Our data, thus, provide evidence for a decisive role of NO in the recovery process of mitochondrial ion transporters function during immersion stress, confirming a direct differential role of NO in mitochondrial ion homeostasis in teleost brain.

Fishes have evolved complex and multi-step physiological mechanisms to drive ion homeostasis in challenging environments. Induction of stress that disturbs ion homeostasis in fishes evokes recovery response for their survival. Nitric Oxide (NO) as gasotransmitter modulates many physiological mechanisms including ion transport in osmoregulatory epithelia in teleosts. However, little is known about the role of NO in the transport of H+ ions that creates proton gradient with the help of H+-dependent ATPases like H+-ATPase and H+/K+-ATPase, particularly in hepatic and cardiac tissues of bony fish. We, thus, quantified H+-ATPase and H+/K+-ATPase in these tissues after in vivo treatments of NO donor, Sodium Nitro-Prusside (SNP) or NOS inhibitor, L-NAME, in both non-stressed and immersion-stressed air-breathing fish, Anabas testudineus Bloch. We found that elevated NO availability by SNP treatment lowered H+-ATPase-driven H+ transport in both hepatic and cardiac tissues of immersion-stressed fish. In contrast, NO depletion by L-NAME treatment elevated H+-ATPase activity in these tissues of stressed fish, pointing to a direct role of H+-ATPase in NO-mediated proton gradient regulation during stress condition. H+/K+-ATPase that drives H+ transport against K+ reduced its activity in cardiac tissue by SNP and L-NAME treatments. But L-NAME treatment in stressed fish imposed a higher H+ transport in cardiac tissue of these fish. Overall, the data indicate that NO has a vital role in the regulation of H+-ATPase-driven proton gradient in both cardiac and hepatic tissues of immersion-stressed fish.

The neuronal circuitries of brain and the corresponding ion transporters contribute to the maintenance of ion homeostasis in fish brain. The sensitivity of these neuronal clusters in response to environmental clues brings neural plasticity and subsequent regulation of stress acclimation. Nitric oxide (NO), a gasotransmitter, is involved in ion transport in many peripheral tissues of fishes including air-breathing fish. However, the role of NO in mitochondrial ion transporter activity has not yet been investigated in fish brain. We, therefore, investigated the short-term in vivo action of a NO donor, Sodium Nitro-Prusside (SNP), on mitochondrial ion transporters such as H+- Ca2+- and Mg2+-dependent ATPases in brain segments such as Prosen-Cephalon (PC), Mesen-Cephalon (MC) and Meten-Cephalon (MeC) of immersion-stressed Anabas testudineus. Intraperitoneal injection of SNP for 30 min lowered the activities of bafilomycin-sensitive H+ATPase and vanadate sensitive Ca2+ATPase in PC, whereas in MeC, these transporters showed significant rise in activities after SNP treatment. The oligomycin-sensitive Mg2+ATPase activity showed a significant decrease in PC and MC of brain after SNP treatment in non-stressed fish. Induction of stress by water immersion altered the activities of these ion transporter activities. However, the treatment of SNP in immersed fish showed recovery of the immersion-induced modulation in the activities of these mitochondrial ion transporters. Our data, thus, provide evidence for a decisive role of NO in the recovery process of mitochondrial ion transporters function during immersion stress, confirming a direct differential role of NO in mitochondrial ion homeostasis in teleost brain.

Fishes have evolved complex and multi-step physiological mechanisms to drive ion homeostasis in challenging environments. Induction of stress that disturbs ion homeostasis in fishes evokes recovery response for their survival. Nitric Oxide (NO) as gasotransmitter modulates many physiological mechanisms including ion transport in osmoregulatory epithelia in teleosts. However, little is known about the role of NO in the transport of H+ ions that creates proton gradient with the help of H+-dependent ATPases like H+-ATPase and H+/K+-ATPase, particularly in hepatic and cardiac tissues of bony fish. We, thus, quantified H+-ATPase and H+/K+-ATPase in these tissues after in vivo treatments of NO donor, Sodium Nitro-Prusside (SNP) or NOS inhibitor, L-NAME, in both non-stressed and immersion-stressed air-breathing fish, Anabas testudineus Bloch. We found that elevated NO availability by SNP treatment lowered H+-ATPase-driven H+ transport in both hepatic and cardiac tissues of immersion-stressed fish. In contrast, NO depletion by L-NAME treatment elevated H+-ATPase activity in these tissues of stressed fish, pointing to a direct role of H+-ATPase in NO-mediated proton gradient regulation during stress condition. H+/K+-ATPase that drives H+ transport against K+ reduced its activity in cardiac tissue by SNP and L-NAME treatments. But L-NAME treatment in stressed fish imposed a higher H+ transport in cardiac tissue of these fish. Overall, the data indicate that NO has a vital role in the regulation of H+-ATPase-driven proton gradient in both cardiac and hepatic tissues of immersion-stressed fish.