Mechanisms underlying the acceleration of thyroid hormone-induced tadpole metamorphosis by corticosterone.
Adrenal steroids have been shown to accelerate both spontaneous and thyroid hormone (TH)-induced metamorphosis. The present study is concerned with the mechanisms underlying this effect. Premetamorphic Rana catesbeiana tadpoles were immersed in water containing 1-20 nM T4 or T3 +/- 1 microM corticosterone (B) for 6 to 19 days. B is the predominant glucocorticoid in tadpole plasma before climax. As indicated by the rate of tail resorption and hepatic carbamyl phosphate synthetase (CPS) activity, metamorphosis was significantly accelerated when TH-treated animals also received B: after 14 days in T4 (20 nM), tadpole tail length was decreased by 10%; in T4 + B, the decrease was 19%. At the same time, CPS activity was increased approximately 12-fold in tadpoles in T4 and 18-fold in those in T4 + B. Comparable results were obtained when T3 was employed. Neither tail resorption nor CPS activity was influenced by B alone. Plasma T4 levels attained at all bath concentrations of T4 were increased more than 2-fold when B was present. The same was true when T3 was used. In addition, in tadpoles immersed in 20 nM T4, the plasma T3 level-was significantly increased in the presence of B. Assessment of 5'-deiodinase and 5-deiodinase activities in vitro revealed that administration of B for 7 days resulted in a significant increase in 5'-deiodinase activity in skin and a significant reduction in T3 5-deiodinase activity in both liver and gut. Treatment with B reduced the rate of turnover of T3; 72 h after injection of 0.01 nmol [125I]T3, B-treated tadpoles had retained approximately 58% of the dose vs. 42% in controls. T3 nuclear receptor number (sites per nucleus) as assessed by an in vitro saturation technique was not altered in liver, tail, or red blood cells after 14 days of exposure to B. On the basis of these findings it is suggested that the acceleration of TH-induced metamorphosis by B is due at least in part to its ability to increase the plasma level of T4 or T3 through its effects on the peripheral metabolism of TH. HD-09020
Galton
V A
VA
Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03756.
D000818:Animals; D002467:Cell Nucleus / Q000378:metabolism; D003345:Corticosterone / Q000494:pharmacology*; D004357:Drug Synergism; D004912:Erythrocytes / Q000378:metabolism; D007453:Iodide Peroxidase / Q000097:blood; D007700:Kinetics; D008099:Liver / Q000378:metabolism; D008675:Metamorphosis, Biological / Q000187:drug effects*; D009132:Muscles / Q000378:metabolism; D011892:Rana catesbeiana; D011988:Receptors, Thyroid Hormone / Q000378:metabolism*; D013974:Thyroxine / Q000097:blood / Q000494:pharmacology*; D014284:Triiodothyronine / Q000097:blood
D011988:Receptors, Thyroid Hormone; D014284:Triiodothyronine; D007453:Iodide Peroxidase; D013974:Thyroxine; D003345:Corticosterone