Intrathyroidally generated iodide: the role of transport in its utilization

Thyroid iodide labeled 72 h earlier with 131I was separated from organic iodine by polyacrylamide gel electrophoresis. The concentration of thyroid radioiodide was not significantly diminished 2 h after the administration of perchlorate (100 mg NaClO4) alone, but perchlorate reduced the rise in glandular radioiodide caused by simultaneously given TSH (1 IU). When propylthiouracil (PTU; 20 mg) was given along with it, perchlorate decreased thyroid radioiodide even in rats not treated with TSH. In rats given perchlorate, PTU caused a much slighter augmentation of the TSH-induced increase in the thyroid radioiodide concentration than in the absence of perchlorate. These results are interpreted as follows. Perchlorate-discharged iodide in rats not given TSH is largely transported iodide. Perchlorate can discharge intrathyroidally generated (internal) iodide too, but this is unequivocally reflected by a decrease in the thyroid iodide concentration only when the production of internal iodide is enhanced by TSH. Perchlorate in its own right interferes with organic binding of internal iodide, thereby partially preempting the effect whereby PTU causes accumulation of internal iodide in TSH-treated rats. We suggest that internal thyroid iodide is transported from its site of generation, the follicular cell, to its site of organic binding, the follicular lumen, by perchlorate-sensitive transport. It is also possible that internal iodide escaping from a follicle is conserved by perchlorate-inhibitable reuptake into follicular cells closer to the venous end of the capillary bed.