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中文摘要：
目的观察不同水平的碘摄人对大鼠碘代谢及相关基因表达的影响。方法Wistar大鼠按体质量、性别随机分为低碘组（LI）、适碘组（NI）、5倍碘组（5HI）、10倍碘组（10HI）、50倍碘组（50HI）、100倍碘组（100HI），分别饮用含碘（碘化钾）量不同的水，饲养12个月后处死，采用RT—PCR及酸消化砷铈催化分光光度法检测甲状腺钠碘转运体（NIS）、氯碘转运体（PDS基因编码）mRNA的表达和尿碘、甲状腺组织含碘量。结果U组尿碘（0μg／L）、甲状腺组织含碘量[（0．0l±0．00）mg／g]显著低于NI组[234．5μg／L、（1．40±0．35）mg／g]，组间比较差异有统计学意义（尸〈0．01）；5HI、10HI、50HI、100HI组尿碘呈成倍升高，甲状腺组织含碘量呈逐渐升高的趋势。均高于NI组（P〈0．01）。U组甲状腺NISmRNA表达水平（1．15±0．16）明显高于NI组（1．11±0．21），组间比较差异有统计学意义（P〈0．01）；5HI、10HI、50HI、100HI组呈逐渐下降趋势，与NI组比较差异有统计学意义（P〈0．01）。PDSmRNA水平，U组和5HI、10HI、50HI、100HI组均高于NI组，但仅U组（1．38±0．39）、50HI组（1．10±0．30）和100HI组（1.02±0．50）与NI组（0．79±0．14）比较差异有统计学意义（p〈0．05）。结论大鼠对长期碘过量比碘缺乏有更强的耐受力，NISmRNA的低表达是机体耐受碘过量的主要机制。碘过量可促进PDSmRNA的表达，这可能与碘过量时甲状腺组织含碘量增加，甲状腺球蛋白（取）发生过度碘化，进而诱发自身免疫反应增强的发病机制有关。
英文摘要：
Objective To explore the effects of the different iodine intake on iodine metabolism and related gene expression at rats. Methods Wistar rats were divided into low iodine （LI）, normal iodine （NI）, five fold iodine （5HI）, ten-fold iodine（10HI）, fifty-fold iodine （50HI）, one hundred-fold iodine （100HI）. Rats in each group drank tap water containing potassium iodide with different concentration. 12 months after after administration, they were then sacrificed. Urinary iodine, thyroid tissue iodine and sodium iodide symporter （NIS）, pendred＇s syndrome（PDS） mRNA were measured. Results Urinary iodine and thyroid iodine content in LI group [0 μg/L, （0.01 ± 0.00）mg/g] were significantly lower than those in NI group[234.5μg/L, （1.40 ± 0.35）mg/g], the difference had statistical significances （P 〈 0.01）. The excessive iodine groups （HI） had significantly high urinary iodine. Thyroid tissue iodine in HI was higher than that in NI （P 〈 0.01 ）. Thyroid NIS expression in LI （1.15 ± 0.16） was higher than that in NI （1.11 ± 0.21 ）, the difference had statistical significance（P 〈 0.01）, and decreased gradually from 5HI to 100HI. The expressions of PDS mRNA in both LI and HI groups were higher than that in NI. However, they were significantly different only in LI （1.38 ± 0.39）, 50HI（1.10 ± 0.30） and 100HI（1.02 ± 0.50） from that in NI（0.79 ± 0.14）, the difference had statistical significances （P 〈 0.05 ）. Conclusions Rats are more tolerant to iodine excess than to iodine deficiency. The down regulation of NIS mRNA is the main mechanism of thyroid being tolerate to iodine excess. Iodine excess can promote PDS mRNA expression, which may be related with the increase of iodine content in thyroid tissue, over-iodization of thyroglobulin （Tg） and the enhance of auto-immunol reactivity when iodine intake is excess.
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