This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints, Permissions and Rights Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by BELSHAW, B. E. Articles by BECKER, D. V. Search for Related Content PubMed PubMed Citation Articles by BELSHAW, B. E. Articles by BECKER, D. V.

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

Department of Medicine, New York Hospital, Cornell University Medical Center New York, New York 10021

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 5 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.

¹ Parts of this work were reported at the meeting of the American Thyroid Association, Birmingham, Alabama, October 14, 1971.

This work was supported in part by grants from the U.S. Atomic Energy Commission (Contract No. AT(30-l)4048) and the Morris Animal Foundation. Reprints: B. E. Belshaw, Division of Nuclear Medicine, New York Hospital, Cornell University Medical Center, 525 East 68th Street, New York, N.Y., 10021.

Received June 19, 1972.

This article has been cited by other articles:

				S. Poncin, A.-C. Gerard, M. Boucquey, M. Senou, P. B. Calderon, B. Knoops, B. Lengele, M.-C. Many, and I. M. Colin Oxidative Stress in the Thyroid Gland: From Harmlessness to Hazard Depending on the Iodine Content Endocrinology, January 1, 2008; 149(1): 424 - 433. [Abstract] [Full Text] [PDF]

				L. Zhang, S. Sharma, L. X. Zhu, T. Kogai, J. M. Hershman, G. A. Brent, S. M. Dubinett, and M. Huang Nonradioactive Iodide Effectively Induces Apoptosis in Genetically Modified Lung Cancer Cells Cancer Res., August 15, 2003; 63(16): 5065 - 5072. [Abstract] [Full Text] [PDF]

				B. Corvilain, L. Collyn, J. van Sande, and J. E. Dumont Stimulation by iodide of H2O2 generation in thyroid slices from several species Am J Physiol Endocrinol Metab, April 1, 2000; 278(4): E692 - E699. [Abstract] [Full Text] [PDF]

				M. Vitale, T. Di Matola, F. D'Ascoli, S. Salzano, F. Bogazzi, G. Fenzi, E. Martino, and G. Rossi Iodide Excess Induces Apoptosis in Thyroid Cells through a p53-Independent Mechanism Involving Oxidative Stress Endocrinology, February 1, 2000; 141(2): 598 - 605. [Abstract] [Full Text] [PDF]

				J. Wolff Perchlorate and the Thyroid Gland Pharmacol. Rev., March 1, 1998; 50(1): 89 - 106. [Abstract] [Full Text] [PDF]