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Several studies have demonstrated that moderately high concentrations of molecular iodine (I2) 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. I2). Further, we show that a moderately high I2supplement (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 I2metabolism is independent of TPO, and we demonstrate that, at the doses used here, which are potentially useful to treat mammary tumors, chronic I2supplement is not accompanied by any harmful secondary effects on the thyroid or general physiology. Thus, we suggest that I2could be considered for use in clinical trials of breast cancer therapies. [ABSTRACT FROM AUTHOR]