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.