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B-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。
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.
出处
《中国地方病学杂志》
CAS
CSCD
北大核心
2006年第3期243-246,共4页
Chinese Jouranl of Endemiology
基金
国家自然科学基金重点项目(30230330)
