Abstract

The hydromineral and metabolic actions of thyroid hormone on osmotic acclimation in fish is less understood. We, therefore, studied the short-term action of triiodothyronine (T 3), the potent thyroid hormone, on the distribution and the function of gill mitochondria-rich (MR) cells and on the whole body hydromineral and metabolic regulations of air-breathing fish ( Anabas testudineus) adapted to either freshwater (FW) or acclimated to seawater (SA; 30 g L −1). As expected, 24 h T 3 injection (100 ng g −1) elevated ( P < 0.05) plasma T 3 but classically reduced ( P < 0.05) plasma T 4. The higher Na +, K +-ATPase immunoreactivity and the varied distribution pattern of MR cells in the gills of T 3-treated FW and SA fish, suggest an action of T 3 on gill MR cell migration, though the density of these cells remained unchanged after T 3 treatment. The ouabain–sensitive Na +, K +-ATPase activity, a measure of hydromineral competence, showed increases ( P < 0.05) in the gills of both FW and SA fish after T 3 administration, but inhibited ( P < 0.05) in the kidney of the FW fish and not in the SA fish. Exogenous T 3 reduced glucose ( P < 0.05) and urea ( P < 0.05) in the plasma of FW fish, whereas these metabolites were elevated ( P < 0.05) in the SA fish, suggesting a modulatory effect of ambient salinity on the T 3-driven metabolic actions. Our data identify gill MR cell as a target for T 3 action as it promotes the spatial distribution and the osmotic function of these cells in both fresh water and in seawater. The results besides confirming the metabolic and osmotic actions of T 3 in fish support the hypothesis that the differential actions of T 3 may be due to the direct influence of ambient salinity, a major environmental determinant that alters the osmotic and metabolic strategies of fish.

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