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BioMed Research International
Volume 2016 (2016), Article ID 1375606, 12 pages
Research Article

Exposure to p,p′-DDE Induces Morphological Changes and Activation of the PKCα-p38-C/EBPβ Pathway in Human Promyelocytic HL-60 Cells

1Departamento de Toxicología, Centro de Investigación y Estudios Avanzados, IPN, Ciudad de México, Mexico
2PIBIOM, ENMH, Instituto Politécnico Nacional, Ciudad de México, Mexico
3Hospital Infantil de México Federico Gómez, SSA, Ciudad de México, Mexico
4Departamento de Bioquímica, Facultad de Medicina, UASLP, San Luis Potosí, SLP, Mexico
5Laboratorio de Inmunología Celular y Molecular, Facultad de Ciencia Químicas, UASLP, San Luis Potosí, SLP, Mexico

Received 24 May 2016; Revised 26 August 2016; Accepted 31 August 2016

Academic Editor: Susan A. Rotenberg

Copyright © 2016 Nallely A. Torres-Avilés 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.


Dichlorodiphenyldichloroethylene (p,p′-DDE), the most persistent metabolite of dichlorodiphenyltrichloroethane (DDT), is still present in the human population. Both are present in the bone marrow of patients with bone marrow disorders, but thus far there are no studies that assess the capability of p,p′-DDE to affect myeloid cells. The aim of this study was to determine the effect of p,p′-DDE on promyelocytic cell differentiation and intracellular pathways related to this event. p,p′-DDE induced morphological changes compatible with promyelocytic differentiation in a concentration-dependent manner. The p,p′-DDE effect on , C/EBPβ protein levels, PKCα and p38 activation, and the role of oxidative stress or PLA2 was assayed. Exposure to 1.9 μg/mL of p,p′-DDE increased , PKCα, p38, and C/EBPβ protein levels; the increase of nuclear C/EBPβ protein was dependent on p38. PKCα phosphorylation was dependent on PLA2 and p,p′-DDE-induced oxidative stress. p38 phosphorylation induced by p,p′-DDE was dependent on PLA2, PKC activation, and oxidative stress. These effects of p,p′-DDE at concentrations found in human bone marrow may induce alterations in immature myeloid cells and could affect their cellular homeostasis. In order to establish the risk from exposure to p,p′-DDE on the development of bone marrow disorders in humans, these effects deserve further study.