Underlying mechanisms of pituitary-thyroid axis function disruption by chronic iodine excess in rats.

Research paper by Jamile J Calil Silveira, Caroline C Serrano do Nascimento, Raquel R Cardoso Laconca, Letícia L Schmiedecke, Rafael R Barrera Salgueiro, Ayrton A Kimidi Kondo, Maria Tereza MT Nunes

Indexed on: 28 Jul '16Published on: 28 Jul '16Published in: Thyroid : official journal of the American Thyroid Association


Iodine is essential for thyroid hormone synthesis and is an important regulator of thyroid function. Chronic iodine deficiency leads to hypothyroidism, but iodine excess also impairs thyroid function causing hyperthyroidism, hypothyroidism and/or thyroiditis. This study aimed to investigate the underlying mechanisms by which exposure to chronic iodine excess impairs pituitary-thyroid axis function.Male Wistar rats were treated for 2 months with NaI (0.05% and 0.005%) or NaI+NaClO4 (0.05%) dissolved in drinking water. Hormone levels, gene expression and thyroid morphology were analyzed later.NaI-treated rats presented high levels of iodine in urine, increased serum TSH (thyroid-stimulating hormone) levels, slightly decreased serum T4/T3 levels and a decreased expression of Nis (sodium/iodide symporter), Tshr (thyroid stimulating hormone receptor) and Tpo (thyroperoxidase) mRNA and protein, suggesting a primary thyroid dysfunction. In contrast, Tg (thyroglobulin) and Pds (pendrin) mRNA and protein content were increased. Kidney and liver Dio1 (deiodinase type 1) mRNA expression was decreased in iodine-treated rats. Morphological studies showed larger thyroid follicles with higher amounts of colloid and increased amounts of connective tissue in the thyroid of iodine-treated animals. All these effects were prevented when perchlorate treatment was combined with iodine excess.Our data reinforce and add novel findings about the disruption of thyroid gland function and the compensatory action of increased TSH levels in iodine-exposed animals. Moreover, they draw attention to the fact that iodine intake should be carefully monitored, since both deficient and excessive ingestion of this trace element may induce pituitary-thyroid axis dysfunction.