title: Uptake and gene expression with antitumoral doses of iodine in thyroid and mammary gland: evidence that chronic administration has no harmful effects.
abstract: Several studies have demonstrated that moderately high concentrations of molecular iodine (I(2)) diminish the symptoms of mammary fibrosis in women, reduce the occurrence of mammary cancer induced chemically in rats (50-70%), and have a clear antiproliferative and apoptotic effect in the human tumoral mammary cell line MCF-7. Nevertheless, the importance of these effects has been underestimated, in part because of the notion that exposure to excess iodine represents a potential risk to thyroid physiology. In the present work we demonstrate that uptake and metabolism of iodine differ in an organ-specific manner and also depend on the chemical form of the iodine ingested (potassium iodide vs. I(2)). Further, we show that a moderately high I(2) supplement (0.05%) causes some of the characteristics of the "acute Wolff-Chaikoff effect"; namely, it lowers expression of the sodium/iodide symporter, pendrin, thyroperoxidase (TPO), and deiodinase type 1 in thyroid gland without diminishing circulating levels of thyroid hormone. Finally, we confirm that I(2) metabolism is independent of TPO, and we demonstrate that, at the doses used here, which are potentially useful to treat mammary tumors, chronic I(2) supplement is not accompanied by any harmful secondary effects on the thyroid or general physiology. Thus, we suggest that I(2) could be considered for use in clinical trials of breast cancer therapies.
authors.affiliation: Instituto de Neurobiología, Universidad Nacional Autónoma de México, Campus UNAM-Juriquilla, Querétaro, México.
authors.forename: Brenda
authors.initials: B
authors.lastname: Anguiano
authors.forename: Pablo
authors.initials: P
authors.lastname: García-Solís
authors.forename: Guadalupe
authors.initials: G
authors.lastname: Delgado
authors.forename: Carmen
authors.initials: C
authors.lastname: Aceves Velasco
mesh_terms: D000818:Animals; D027963:Chloride-Bicarbonate Antiporters / Q000096:biosynthesis; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D007453:Iodide Peroxidase / Q000096:biosynthesis; D007455:Iodine / Q000378:metabolism* / Q000494:pharmacology* / Q000627:therapeutic use; D007457:Iodine Radioisotopes; D007784:Lactoperoxidase / Q000096:biosynthesis; D008321:Mammary Glands, Animal / Q000187:drug effects / Q000378:metabolism*; D015674:Mammary Neoplasms, Animal / Q000188:drug therapy / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D000076988:Sulfate Transporters; D027981:Symporters / Q000096:biosynthesis; D013961:Thyroid Gland / Q000187:drug effects / Q000378:metabolism*; D013963:Thyroid Hormones / Q000097:blood; D000099209:Sodium-Iodide Symporters
chemical_list: D027963:Chloride-Bicarbonate Antiporters; D007453:Iodide Peroxidase; D007455:Iodine; D007457:Iodine Radioisotopes; D007784:Lactoperoxidase; D000076988:Sulfate Transporters; D027981:Symporters; D013963:Thyroid Hormones; D000099209:Sodium-Iodide Symporters; C494615:Slc26A4 protein, rat