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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 Google Scholar Articles by Arroyo-Helguera, O Articles by Aceves, C 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.