This Article Full Text Full Text (PDF) Alert me when this article is cited 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 Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Contempré, B. Articles by Many, M.-C. Search for Related Content PubMed PubMed Citation Articles by Contempré, B. Articles by Many, M.-C.

Thiocyanate Induces Cell Necrosis and Fibrosis in Selenium- and Iodine-Deficient Rat Thyroids: A Potential Experimental Model for Myxedematous Endemic Cretinism in Central Africa

Institute of Interdisciplinary Research (B.C., J.E.D.), Laboratory of Clinical Biology (B.C.), and Laboratory of Epidemiology (B.C.), Free University of Brussels; Laboratory of Histology, Catholic University of Louvain (J.-F.D., M.-C.M.), Brussels, Belgium; and Instituto de Investigationes Biomedicas Arturo Duperier (G.M.d.E.), Madrid, Spain

Address all correspondence and requests for reprints to: Prof. M.-C. Many, Université Catholique de Louvain, Medical School, Histology Unit, UCL-5229, avenue E. Mounier, B-1200 Brussels, Belgium. E-mail: many{at}isto.ucl.ac.be.

Thyroid destruction leading to endemic myxoedematous cretinism is highly prevalent in central Africa, where iodine (I) and selenium (SE) deficiencies as well as thiocyanate (SCN) overload are combined. All three factors have been studied experimentally in the etiology of the disease, but they have never been studied in combination. In a model using rats, we have previously shown that combining I and SE deficiencies increases the sensitivity of the thyroid to necrosis after iodide overload, an event unlikely to occur in the African situation. To develop a model that would more closely fit with the epidemiological findings, we have determined whether an SCN overload would also result in thyroid necrosis as does the I overload. The combination of the three factors increased by 3.5 times the amount of necrotic cells, from 5.5 ± 0.3% in the I^-SE⁺ thyroids to 18.9 ± 1.6% in the I^-SE^-SCN-overloaded ones. Methimazole administration prevented the SCN-induced necrosis. SE^- thyroids evolved to fibrosis, whereas SE⁺ thyroids did not. TGFß was prominent in macrophages present in SE^- glands. Thyroid destruction in central Africa might therefore originate from the interaction of three factors: I and SE deficiencies by increasing H₂O₂ accumulation, SE deficiency by decreasing cell defense and promoting fibrosis, and SCN overload by triggering follicular cell necrosis.

This article has been cited by other articles:

				N. Driessens, S. Versteyhe, C. Ghaddhab, A. Burniat, X. De Deken, J. Van Sande, J.-E. Dumont, F. Miot, and B. Corvilain Hydrogen peroxide induces DNA single- and double-strand breaks in thyroid cells and is therefore a potential mutagen for this organ Endocr. Relat. Cancer, September 1, 2009; 16(3): 845 - 856. [Abstract] [Full Text] [PDF]

				S. Poncin, I. M Colin, and A.-C. Gerard Minimal oxidative load: a prerequisite for thyroid cell function J. Endocrinol., April 1, 2009; 201(1): 161 - 167. [Abstract] [Full Text] [PDF]

				P. J Obendorf, C. E Oxnard, and B. J Kefford Are the small human-like fossils found on Flores human endemic cretins? Proc R Soc B, June 7, 2008; 275(1640): 1287 - 1296. [Abstract] [Full Text] [PDF]

				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]

				Y. Song, N. Driessens, M. Costa, X. De Deken, V. Detours, B. Corvilain, C. Maenhaut, F. Miot, J. Van Sande, M.-C. Many, et al. Roles of Hydrogen Peroxide in Thyroid Physiology and Disease J. Clin. Endocrinol. Metab., October 1, 2007; 92(10): 3764 - 3773. [Abstract] [Full Text] [PDF]

				P. E. Pedraza, M.-J. Obregon, H. F. Escobar-Morreale, F. Escobar del Rey, and G. M. de Escobar Mechanisms of Adaptation to Iodine Deficiency in Rats: Thyroid Status Is Tissue Specific. Its Relevance for Man Endocrinology, May 1, 2006; 147(5): 2098 - 2108. [Abstract] [Full Text] [PDF]

				L. Schomburg, C. Riese, M. Michaelis, E. Griebert, M. O. Klein, R. Sapin, U. Schweizer, and J. Kohrle Synthesis and Metabolism of Thyroid Hormones Is Preferentially Maintained in Selenium-Deficient Transgenic Mice Endocrinology, March 1, 2006; 147(3): 1306 - 1313. [Abstract] [Full Text] [PDF]

				J. Kohrle, F. Jakob, B. Contempre, and J. E. Dumont Selenium, the Thyroid, and the Endocrine System Endocr. Rev., December 1, 2005; 26(7): 944 - 984. [Abstract] [Full Text] [PDF]