The Effect on Sodium/Iodide Symporter and Pendrin in Thyroid Colloid Retention Developed by Excess Iodide Intake
The Effect on Sodium/Iodide Symporter and Pendrin in Thyroid Colloid Retention Developed by Excess Iodide Intake
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DOI：
10.1007/s12011-015-0580-4
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发表时间：
2016-07-01
影响因子：
3.9
通讯作者：
Lei, Yi-xiong
中科院分区：
文献类型：
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作者：
Chen, Xiao-yi;Lin, Chu-hui;Lei, Yi-xiong
众所周知，过量的碘可导致甲状腺胶体潴留，这是碘致甲状腺肿的典型特征。然而，该机制尚未完全揭示。碘在甲状腺胶体合成和转运的多个步骤中发挥重要作用，其中钠/碘同向转运体（NIS）和pendrin是必不可少的。本研究以不同浓度的高碘水喂养雌性BALB B/c小鼠，包括A组（对照组，0 μ g/L）、B组（1500 μ g/L）、C组（3000 μ g/L）、D组（6000 μ g/L）和E组（12,000 μ g/L）。喂养7个月后，我们发现过量碘可导致不同程度的甲状腺胶体潴留。高剂量组NIS和pendrin表达下调。尿碘测定和甲状腺I-125实验测定的甲状腺摄碘功能表明，随着饮水中碘浓度的增加，尿碘含量增加，而摄碘率降低（与对照组相比均P < 0.05）。此外，透射电子显微镜（TEM）显示甲状腺细胞内线粒体数量减少。基于这些发现，我们得出结论，过量碘加剧甲状腺胶体潴留的发生与NIS和pendrin表达的抑制有关，这为过量碘对甲状腺的潜在作用机制提供了额外的见解。
It is well known that excess iodide can lead to thyroid colloid retention, a classic characteristic of iodide-induced goiter. However, the mechanism has not been fully unrevealed. Iodide plays an important role in thyroid function at multiple steps of thyroid colloid synthesis and transport among which sodium/iodide symporter (NIS) and pendrin are essential. In our study, we fed female BALB/c mice with different concentrations of high-iodine water including group A (control group, 0 mu g/L), group B (1500 mu g/L), group C (3000 mu g/L), group D (6000 mu g/L), and group E (12,000 mu g/L). After 7 months of feeding, we found that excess iodide could lead to different degrees of thyroid colloid retention. Besides, NIS and pendrin expression were downregulated in the highest dose group. The thyroid iodide intake function detected by urine iodine assay and thyroidal I-125 experiments showed that the urine level of iodine increased, while the iodine intake rate decreased when the concentration of iodide used in feeding water increased (all p < 0.05 vs. control group). In addition, transmission electron microscopy (TEM) indicated a reduction in the number of intracellular mitochondria of thyroid cells. Based on these findings, we concluded that the occurrence of thyroid colloid retention exacerbated by excess iodide was associated with the suppression of NIS and pendrin expression, providing an additional insight of the potential mechanism of action of excess iodide on thyroid gland.