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中文摘要：
目的研究不同碘营养状态对大鼠肝组织甲腺氨酸Ⅰ型5′脱碘酶（DI）表达水平及活性的影响。方法正常1月龄Wistar大鼠根据碘摄入量不同分为6组，饲养3个月后处死。放免法测定血清甲状腺激素水平。提取肝组织总RNA，以β—actin为内对照，半定量RT-PCR分析DI基因的表达水平。Chopra氏方法测定肝组织匀浆液中DI的脱碘活性。结果LI组TT4和FT4显著低于其他5组（P〈0．05），100HI组TT3和FT3显著低于其他5组（P〈0．05），100HI组TT4和FT4显著低于NI、5HI、10HI和50HI组（P〈0．05）。大鼠肝组织DI基因mRNA表达量6组间差异有统计学意义（P〈0．01），LI组显著高于其他5组（P〈0．05），不同剂量HI组和NI组相比差异均无统计学意义（P〉0．05）。大鼠肝组织DI活性6组间差异有统计学意义（P〈0．01），LI组显著高于其他5组（P〈0．05），50HI组和100HI组显著低于其他4个组（P〈0．05）。结论在碘缺乏状态下。大鼠出现以低T4为主要表现的甲状腺功能减退（甲减），DI活性和DI基因表达水平代偿性上调，使机体维持足够的T3水平，以避免周围组织出现器官性甲减。高碘仅在转录后水平影响DI，表现为直接抑制DI的活性。使血清TT3和FT3下降，机体出现失代偿性周围组织器官性甲减。DI对碘过量有一定的耐受能力，这种耐受性有一定的阈值。
英文摘要：
Objective To study the influence of iodine nutrition on the activity and gene expressing level of type Ⅰ iodothyronine deiodinase （DI） in rat liver. Methods 1-month aged normal Wistar rats were randomly divided into 6 groups according to deferent iodine intakes and all rats were killed 3 months afterwards. Concentration of thyroid hormone in serum was assayed with radioimmunoassay. DI gene expressing level was tested by semiquantitative RT-PCR meanwhile the activity of DI was also tested with Chopra＇s method. Results Serum TT4 and FT4 levels in LI group were lower than that in every other group （P 〈 0.05）. In 100HI group serum FT3 and TT3 levels were lower than that of those 5 groups（P 〈 0.05）, FT4 and TT4 levels were also lower than those of NI, 5HI, 10HI and 50HI groups （P 〈 0.05）. DI gene expressing level had significant differences among the 6 groups （P 〈 0.01）; It was much higher in LI rats than in NI and 4 HI groups （P 〈 0.05）. Although there were no significant differences among NI and those 4 HI groups（P 〉 0.05） but a decreasing tendency was appeared in 50HI and 100HI groups. LI rats had a much higher DI activity than that of NI and 4 HI groups （P 〈 0.05）. On the contrary, DI activity in 50HI and 100HI rats was lower than that in other 4 groups （P 〈 0.05）. Conclusions Hypothyreosis reflected by Ts level decrease happens under the condition of iodine deficiency. Both gene expressing level and the activity of DI in rat liver rises significantly as a compensation in iodine deficiency groups in order to maintain T3 concentration and avoid organogenic hypothyreosis. However, DI can tolerant the excess of iodine to a certain extent, exceedingly high iodine inhibits DI activity other than influences DI at gene level, so organogenic hypothyreosis occurs resulting from the decrease of FT3 and TT3 levels.
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