Ahrén B, Rerup C
Pharmacol Toxicol. 1987 Jul;61(1):69-71. doi: 10.1111/j.1600-0773.1987.tb01776.x.
The kinetics of free and hormone bound blood iodine after stimulation with endogenous thyroid stimulating hormone (TSH) are not satisfactorily characterized. We studied these kinetics in mice injected with 125I and thyroxine. In control mice, the injected 125I is organified within the thyroid and incorporated into thyroid hormones, whereas in mice treated with the thyreostatic drug propylthiouracil (PTU), most 125I remains inorganic, since the thyroperoxidase activity is inhibited by PTU. We found that during blockade of TSH secretion by means of thyroxine, blood 125I activity was significantly higher in PTU-treated animals than in controls, indicating that PTU impaired thyroidal uptake of 125I. On the fourth day after the thyroxine load, the blockade of TSH secretion vanished. This caused the blood 125I activity to increase markedly. The increase of blood 125I was as high in PTU-treated animals as in controls. After the peak, blood 125I was cleared according to first order kinetics, with a half-time of 0.72 days (= 17.3 hours) in PTU-treated animals and of 6.3 days in controls (P less than 0.001). It is suggested (1) that PTU impairs thyroidal uptake of iodide, (2) that endogenous TSH stimulates release from the thyroid of inorganic iodide as well as of thyroid hormones, and (3) that inorganic iodide released by the thyroid has a much shorter biological half-life than hormone-bound iodine.
内源性促甲状腺激素(TSH)刺激后,游离及与激素结合的血碘动力学特征尚未得到充分阐明。我们在注射了125I和甲状腺素的小鼠中研究了这些动力学。在对照小鼠中,注射的125I在甲状腺内有机化并掺入甲状腺激素中,而在用抗甲状腺药物丙硫氧嘧啶(PTU)治疗的小鼠中,由于PTU抑制了甲状腺过氧化物酶活性,大部分125I仍为无机碘。我们发现,在通过甲状腺素阻断TSH分泌期间,PTU处理的动物血125I活性显著高于对照组,表明PTU损害了甲状腺对125I的摄取。在给予甲状腺素负荷后的第四天,TSH分泌的阻断消失。这导致血125I活性显著增加。PTU处理的动物和对照组血125I的增加幅度相同。在达到峰值后,血125I按照一级动力学清除,PTU处理的动物半衰期为0.72天(=17.3小时),对照组为6.3天(P<0.001)。有人提出:(1)PTU损害甲状腺对碘化物的摄取;(2)内源性TSH刺激甲状腺释放无机碘以及甲状腺激素;(3)甲状腺释放的无机碘的生物半衰期比与激素结合的碘短得多。