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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 162876, 11 pages
Research Article

Copper Uptake in Mammary Epithelial Cells Activates Cyclins and Triggers Antioxidant Response

1Center for Natural Sciences and Humanities, Federal University of ABC (UFABC), 09210-170 Santo André, SP, Brazil
2Center for Mathematics, Computation and Cognition, Federal University of ABC (UFABC), 09210-170 Santo André, SP, Brazil

Received 10 March 2015; Accepted 14 June 2015

Academic Editor: Joseph A. Adeyemi

Copyright © 2015 Nathália Villa dos Santos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The toxicologic effects of copper (Cu) on tumor cells have been studied during the past decades, and it is suggested that Cu ion may trigger antiproliferative effects in vitro. However, in normal cells the toxicologic effects of high exposures of free Cu are not well understood. In this work, Cu uptake, the expression of genes associated with cell cycle regulation, and the levels of ROS production and related oxidative processes were evaluated in Cu-treated mammary epithelial MCF10A nontumoral cells. We have shown that the Cu additive is associated with the activation of cyclin D1 and cyclin B1, as well as cyclin-dependent kinase 2 (CDK2). These nontumor cells respond to Cu-induced changes in the oxidative balance by increase of the levels of reduced intracellular glutathione (GSH), decrease of reactive oxygen species (ROS) generation, and accumulation during progression of the cell cycle, thus preventing the cell abnormal proliferation or death. Taken together, our findings revealed an effect that contributes to prevent a possible damage of normal cells exposed to chemotherapeutic effects of drugs containing the Cu ion.