Chen Xiao-Yi, Lin Chu-Hui, Yang Li-Hua, Li Wang-Gen, Zhang Jin-Wei, Zheng Wen-Wei, Wang Xiang, Qian Jiang, Huang Jia-Luan, Lei Yi-Xiong
School of Public Health, Guangzhou Medical University, 195 Dongfengxi Road, Guangzhou, 510182, People's Republic of China.
Department of Endocrinology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510260, People's Republic of China.
Biol Trace Elem Res. 2016 Jul;172(1):193-200. doi: 10.1007/s12011-015-0580-4. Epub 2015 Dec 11.
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 μg/L), group B (1500 μg/L), group C (3000 μg/L), group D (6000 μg/L), and group E (12,000 μg/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 (125)I 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.
众所周知，过量碘可导致甲状腺胶体潴留，这是碘致甲状腺肿的一个典型特征。然而，其机制尚未完全阐明。碘在甲状腺胶体合成和运输的多个步骤中对甲状腺功能起着重要作用，其中钠/碘同向转运体（NIS）和pendrin至关重要。在我们的研究中，我们用不同浓度的高碘水喂养雌性BALB/c小鼠，包括A组（对照组，0μg/L）、B组（1500μg/L）、C组（3000μg/L）、D组（6000μg/L）和E组（12000μg/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。此外，最高剂量组中NIS和pendrin的表达下调。通过尿碘测定和甲状腺（125）I实验检测的甲状腺碘摄取功能表明，当喂养水中碘的浓度增加时，尿碘水平升高，而碘摄取率降低（与对照组相比，所有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，过量碘加剧的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作用的潜在机制提供了新的见解。
