Lisbôa P C, Curty F H, Moreira R M, Pazos-Moura C C
Laboratório de Fisiologia Endócrina, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brasil.
Braz J Med Biol Res. 1997 Dec;30(12):1479-84. doi: 10.1590/s0100-879x1997001200016.
There is little information on the possible effects of estrogen on the activity of 5'-deiodinase (5'-ID), an enzyme responsible for the generation of T3, the biologically active thyroid hormone. In the present study, anterior pituitary sonicates or hepatic and thyroid microsomes from ovariectomized (OVX) rats treated or not with estradiol benzoate (EB, 0.7 or 14 micrograms/100 g body weight, s.c., for 10 days) were assayed for type I 5'-ID (5'-ID-I) and type II 5'-ID (5'-ID-II, only in pituitary) activities. The 5'-ID activity was evaluated by the release of 125I from deiodinated 125I rT3, using specific assay conditions for type I or type II. Serum TSH and free T3 and free T4 were measured by radioimmunoassay. OVX alone induced a reduction in pituitary 5'-ID-I (control = 723.7 +/- 67.9 vs OVX = 413.9 +/- 26.9; P < 0.05), while the EB-treated OVX group showed activity similar to that of the normal group. Thyroid 5'-ID-I showed the same pattern of changes, but these changes were not statistically significant. Pituitary and hepatic 5'-ID-II did not show major alterations. The treatment with the higher EB dose (14 micrograms), contrary to the results obtained with the lower dose, had no effect on the reduced pituitary 5'-ID-I of OVX rats. However, it induced an important increment of 5'-ID-I in the thyroid gland (0.8 times higher than that of the normal group: control = 131.9 +/- 23.7 vs OVX + EB 14 micrograms = 248.0 +/- 31.2; P < 0.05), which is associated with increased serum TSH (0.6-fold vs OVX, P < 0.05) but normal serum free T3 and free T4. The data suggest that estrogen is a physiological stimulator of anterior pituitary 5'-ID-I and a potent stimulator of the thyroid enzyme when employed at high doses.
关于雌激素对5'-脱碘酶（5'-ID）活性可能产生的影响，目前所知甚少。5'-ID是一种负责生成生物活性甲状腺激素T3的酶。在本研究中，对去卵巢（OVX）大鼠（皮下注射苯甲酸雌二醇（EB，0.7或14微克/100克体重，持续10天）或未接受该处理）的垂体前叶超声匀浆、肝脏和甲状腺微粒体进行了I型5'-ID（5'-ID-I）和II型5'-ID（仅在垂体中存在的5'-ID-II）活性检测。5'-ID活性通过从脱碘的125I反T3中释放125I来评估，采用针对I型或II型的特定检测条件。通过放射免疫分析法测定血清促甲状腺激素（TSH）以及游离T3和游离T4。单独的OVX处理导致垂体5'-ID-I活性降低（对照组 = 723.7±67.9，OVX组 = 413.9±26.9；P<0.05），而接受EB处理的OVX组显示出与正常组相似的活性。甲状腺5'-ID-I呈现出相同的变化模式，但这些变化无统计学意义。垂体和肝脏中的5'-ID-II未显示出主要改变。与低剂量EB处理的结果相反，高剂量EB（14微克）处理对OVX大鼠垂体中降低的5'-ID-I没有影响。然而，它导致甲状腺中5'-ID-I显著增加（比正常组高0.8倍：对照组 = 131.9±23.7，OVX + EB 14微克组 = 248.0±31.2；P<0.05），这与血清TSH升高（相对于OVX组升高0.6倍，P<0.05）相关，但血清游离T3和游离T4正常。数据表明，雌激素是垂体前叶5'-ID-I的生理刺激剂，高剂量使用时是甲状腺该酶的强效刺激剂。
