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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 [Ca 2+ ] i , C/EBP β  protein levels, PKC α  and p38 activation, and the role of oxidative stress or PLA2 was assayed. Exposure to 1.9  μ g/mL of  p , p ′-DDE increased [Ca 2+ ] i , PKC α , p38, and C/EBP β  protein levels; the increase of nuclear C/EBP β  protein was dependent on p38. PKC α  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.

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