Dupont A, Labrie F, Levasseur L, Dussault J H, Schally A V
Clin Endocrinol (Oxf). 1976 Jul;5(4):323-30. doi: 10.1111/j.1365-2265.1976.tb01961.x.
The inactivation of synthetic [3H]thyrotrophin-releasing hormone (TRH) by plasma was studied in rats treated with propylthiouracil (PTU) alone or with PTU and thyroxine. 48 h after the onset of treatment with thyroxine, the capacity of rat plasma to inactivate [3H]TRH was significantly increased. The percentage of deamidation of TRH to TRH-free acid was increased 2-fold after 4 days of administration of thyroid hormone. The inactivation of TRH by plasma from hypothyroid patients was compared to that obtained from hyperthyroid patients. Extraction of human plasma incubated with [3H]TRH, followed by thin-layer electrophoresis, showed that transformation of [3H[TRH into TRH-free acid was 44% higher in plasma from hyperthyroid than from hypothyroid patients (P less than 0-05). These data suggest that the inactivation process of TRH by blood proteins could be an important factor in the regulation of the hypothalamo-hypophyseal-thyroid axis in rat and man.
在单独使用丙硫氧嘧啶（PTU）或同时使用PTU和甲状腺素治疗的大鼠中，研究了血浆对合成的[3H]促甲状腺激素释放激素（TRH）的失活作用。甲状腺素治疗开始48小时后，大鼠血浆使[3H]TRH失活的能力显著增强。给予甲状腺激素4天后，TRH脱酰胺生成无TRH酸的百分比增加了2倍。将甲状腺功能减退患者血浆对TRH的失活作用与甲状腺功能亢进患者血浆的进行了比较。用[3H]TRH孵育人血浆，然后进行薄层电泳，结果显示，甲状腺功能亢进患者血浆中[3H]TRH转化为无TRH酸的比例比甲状腺功能减退患者血浆高44%（P<0.05）。这些数据表明，血液蛋白对TRH的失活过程可能是大鼠和人类下丘脑-垂体-甲状腺轴调节中的一个重要因素。
