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Instituto de Neurobiología, Universidad Nacional Autónoma de México, Campus Juriquilla Km 15 Carretera Qro-SLP, Juriquilla, 76230 Querétaro, México

(Requests for offprints should be addressed to C Aceves; Email: caracev{at}servidor.unam.mx)

This study analyzes the uptake and antiproliferative effect of two different chemical forms of iodine, iodide (I^–) and molecular iodine (I₂), in MCF-7 cells, which are inducible for the Na⁺/I^– symporter (NIS) and positive for pendrin (PDS). The mouse fibroblast cell line NIH3T3 was used as control. Our results show that in MCF-7 cells, I^– uptake is sustained and dependent on NIS, whereas I₂ uptake is transient with a maximal peak at 10 min and a final retention of 10% of total uptake. In contrast, no I^– was taken up by NIH3T3 cells, and although I₂ was captured with the same time pattern as in MCF-7 cells, its uptake was significantly lower, and it was not retained within the cell. The uptake of I₂ is independent of NIS, PDS, Na⁺, and energy, but it is saturable and dependent on protein synthesis, suggesting a facilitated diffusion system. Radioiodine was incorporated into protein and lipid fractions only with I₂ treatment. The administration of non-radiolabeled I₂ and 6-iodo-5-hydroxy-8,11,14-eicosatrienoic acid (6-iodolactone, an iodinated arachidonic acid), but not KI, significantly inhibited proliferation of MCF-7 cells. Proliferation of NIH3T3 cells was not inhibited by 20 µM I₂. In conclusion, these results demonstrate that I₂ uptake does not depend on NIS or PDS; they suggest that in mammary cancer cells, I₂ is taken up by a facilitated diffusion system and then covalently bound to lipids or proteins that, in turn, inhibit proliferation.

This article has been cited by other articles:

				O Arroyo-Helguera, E Rojas, G Delgado, and C Aceves Signaling pathways involved in the antiproliferative effect of molecular iodine in normal and tumoral breast cells: evidence that 6-iodolactone mediates apoptotic effects Endocr. Relat. Cancer, December 1, 2008; 15(4): 1003 - 1011. [Abstract] [Full Text] [PDF]