Melatonin integrates multidimensional regulation of Na/K-ATPase in ionocytes and promotes stress and ease response in hypoxia-induced air-breathing fish: lessons from integrative approach.

As circadian regulator, melatonin is involved in many physiological processes including ionosmotic regulation in fishes. Na/K-ATPase (NKA), an ubiquitous Na/K transporter in ionocyte epithelia that drives electrochemical Na gradients and systemic osmotic integration, is a target of stress in fish. However, it is not certain how melatonin regulates NKA functions in ionocyte epithelia and how it modulates the adaptive response such as stress and ease response in fish particularly in hypoxia condition.

Inducible Nitric Oxide Synthase/Nitric Oxide System as a Biomarker for Stress and Ease Response in Fish: Implication on Na Homeostasis During Hypoxia.

The cellular and organismal response to stressor-driven stimuli evokes stress response in vertebrates including fishes. Fishes have evolved varied patterns of stress response, including ionosmotic stress response, due to their sensitivity to both intrinsic and extrinsic stimuli. Fishes that experience hypoxia, a detrimental stressor that imposes systemic and cellular stress response, can evoke disturbed ion homeostasis.

Nitric oxide synthase (NOS) inhibitor L-NAME activates inducible NOS/NO system and drives multidimensional regulation of Na /K -ATPase in ionocyte epithelia of immersion-stressed air-breathing fish (Anabas testudineus Bloch).

Nitric oxide (NO) has been implicated in Na  homeostatic control in water-breathing fishes. It is, however, uncertain whether air-breathing fish relies on NO to coordinate Na /K -ATPase (NKA)-driven Na  transport during acute hypoxemia. We, thus, examined the action of nitric oxide synthase (NOS) inhibitor, L-NAME on NO availability, inducible NOS (iNOS) protein abundance and the regulatory dynamics of NKA in osmoregulatory epithelia of Anabas testudineus kept at induced hypoxemia.