Abstract

SYNOPSIS. Amphibia require thyroid hormone (TH) for larval development and metamorphosis, and secretion of TH by the thyroid gland is greatly increased just before the onset of metamorphic climax. This communication is concerned with changes which occur during development at three potential sites of regulation of TH action at the level of the target cell: the nuclear TH receptor, and the TH 5 monodeiodinase (5 D) and 5′ monodeiodinase (5′D) systems. The nuclear TH receptor was studied in isolated red blood cells (RBCs) and in liver Both tissues were found to contain a single class of putative TH receptors with an affinity for T3 that is at least three times that for T4. In RBCs the number of sites/nucleus increases almost fivefold during development from the premetamorphic stages to the onset of metamorphic climax. This increase was shown to be causally related to the increases in circulating TH levels. In contrast, receptor number in liver does not increase with development and is not influenced by TH. In vivo studies indicate that accumulation of 3,5,3′-triiodothyronine (T3) following administration of thyroxine (T4) is minimal until just prior to metamorphic climax. In vitro studies of 5 D and 5′D activities suggest that this is due primarily to the presence in pre- and prometamorphic tadpole liver of an active 5 D system which rapidly converts any T3, present to 3,3′-diiodothyronine. During climax the activity of this enzyme is minimal and thus T3 can accumulate. These findings are discussed in the light of the current theory of TH action and the known marked differences in the ultimate expression of TH action in RBCs and hepatic tissue during metamorphosis.

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