Acute and Chronic Effects of Iodide on Thyroid Radioiodine Metabolism in Iodine-Deficient Rats¹

Abstract

Work of previous investigators has established that the distribution of 131I among the iodoamino acids of the thyroids of rats on an adequate iodine intake is not seriously affected by a previous acute injection of NaC104, whereas it is markedly altered by acute administration of propylthiouracil (PTU). In iodinedeficient rats, we observed that the administration of NaC104 shortly before injection of carrierfree 131I resulted in a striking further increase in the usual high values for MIT*/DIT/, and in marked decreases in T4/ and T3/. Similar changes were seen after injection of PTU. The effect of NaC104 was completely abolished by administration of 20 /μg of stable iodide together with the 131I. Similarly, in iodine-deficient rats not receiving NaC104, injection of graded doses of iodide carrier (up to 5 μg) with 131I led to progressively greater values for T4/ and DIT/, and to progressively lower values for MIT/ and T3/. These results indicate that the degree of incorporation of stable iodide into thyroglobulin is an important factor in determining the distribution of newly entering iodide among the iodoamino acids of the thyroid. Equilibrium labeling experiments with iodine deficient rats demonstrated that as daily iodine intake increased from 0.3 to 5.3 μg/day, there was a progressive increase in the amount of stable MIT, DIT, T3 and T4 in the thyroid, while MIT/DIT and T3/T4 progressively diminished. Not only the T4 level, but also the molecular ratio, T4/DIT (coupling efficiency), was reduced in thyroids of extremely iodine-deficient rats. This suggests that extreme iodine deficiency reduces thyroid hormone production not only by limiting the availability of iodine, but also by impairing the efficiency of the coupling reaction. A relatively small increase in iodine intake restored coupling efficiency to maximal values, and also resulted in a marked decrease in MIT/DIT. (Endocrinology83: 279, 1968)