Metamorphosis in the Summer Flounder, Paralichthys dentatus: Thyroidal Status Influences Gill Mitochondria-Rich Cells

Metamorphosis in the summer flounder (Paralichthys dentatus) is mediated by thyroid hormones (TH) and is accompanied by changes in gill mitochondria-rich cells (MRCs) and in salinity tolerance. Altered thyroid status during larval development and metamorphosis in this species influences salinity tolerance, though the influence of any hormone on MRCs of larval marine teleosts is not known. This study characterized the effect of altered thyroid status on MRC intracellular membranes, mitochondria size and ultrastructure, immunoreactive (ir)-Na+,K+-ATPase, and cell size and density during metamorphosis in summer flounder. Inhibition of metamorphosis with thiourea (30 ppm) (TU, an inhibitor of TH synthesis) inhibited changes in MRCs, producing large “larval” type MRCs with weak reactivity to osmium; large, electron-lucent mitochondria; and weak ir-Na+,K+-ATPase. Replacement of TH with TU + thyroxine–Na salt (100 ppb) rescued the fish from developmental inhibition, producing smaller “juvenile” type MRCs with strong reactivity to osmium; smaller, electron-opaque mitochondria; and strong ir-Na+,K+-ATPase. The findings suggest that TH are necessary for MRCs to change from larval to juvenile form during metamorphosis.