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This Article Full Text Full Text (PDF) All Versions of this Article: ERC-08-0125v1 15/4/1003    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Arroyo-Helguera, O Articles by Aceves, C Search for Related Content PubMed PubMed Citation Articles by Arroyo-Helguera, O Articles by Aceves, C

Instituto de Neurobiología, Boulevard Juriquilla 3001, Juriquilla, Querétaro 76230¹ Instituto de Investigaciones Biomédicas, Ciudad Universitaria, Universidad Nacional Autónoma de México, D F 04510, México

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

Previous reports have documented the antiproliferative properties of I₂ and the arachidonic acid (AA) derivative 6-iodolactone (6-IL) in both thyroid and mammary glands. In this study, we characterized the cellular pathways activated by these molecules and their effects on cell cycle arrest and apoptosis in normal (MCF-12F) and cancerous (MCF-7) breast cells. Low-to-moderate concentrations of I₂ (10–20 µM) cause G1 and G2/M phase arrest in MCF-12F and caspase-dependent apoptosis in MCF-7 cells. In normal cells, only high doses of I₂ (40 µM) induced apoptosis, and this effect was mediated by poly (ADP-ribose) polymerase-1 (PARP1) and the apoptosis-induced factor, suggesting an oxidative influence of iodine at high concentrations. Our data indicate that both I₂ and 6-IL trigger the same intracellular pathways and suggest that the antineoplasic effect of I₂ in mammary cancer involves the intracellular formation of 6-IL. Mammary cancer cells are known to contain high concentrations of AA, which might explain why I₂ exerts apoptotic effects at lower concentrations only in tumoral cells.