Necrosis of Follicular Cells and Discharge of Thyroidal Iodine Induced by Administering Iodide to Iodine-Deficient Dogs1

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Abstract
The administration of large doses of stable iodide to dogs with natural or experimentally-induced iodine deficiency causes the discharge of prelabeled organic and inorganic iodine from the thyroid. The discharge of thyroidal iodine is manifested by significant elevations in PB131I and serum non-precipitable 131I levels within 12–14 hr after an oral iodide load and by pronounced depletion of stainable colloid in histologic sections of the gland. In some dogs the discharge is preceded or accompanied by necrosis of the epithelium in larger follicles which have vacuolated colloid. The necrosis is evident by as early as 5½ hr after oral administration of 0.5 mg I–/kg or more but is prevented by as little as 0.05 mg I–/kg given 24 hr before the load. Neither C1O4– nor SCN– produce the necrosis in susceptible dogs when given in doses of 2.5 mg/kg. Susceptibility to the cytotoxic effect of excess iodide appears to be related to certain kinetic characteristics of the iodine-deficient gland.