Uptake and gene expression with antitumoral doses of iodine in thyroid and mammary gland:: Evidence that chronic administration has no harmful effects

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.