The organophosphate chlorpyrifos triggers anti-oxidative defense mechanisms in JEG-3 cells

CHIAPELLA GRACIELA; FLORES-MARTÍN JÉSICA; RIDANO, MAGALÍ; REYNA LUCIANA; MAGNARELLI GLADIS; PANZETTA DE DUTARI GRACIELA; GENTI DE RAIMONDI SUSANA

Simposio; V Latin American Symposium on Maternal Fetal Interaction & Placenta; 2013

The organophosphate chlorpyrifos triggers anti-oxidative defense mechanisms in JEG-3 cells Chiapella G1, Flores-Martín J2, Ridano M2, Reyna L2, Panzetta-Dutari G2, Magnarelli G1, Genti-Raimondi S2 1Facultad Ciencias Médicas, IDEPA?CONICET, U.N. del Comahue, Neuquén, Argentina 2CIBICI?CONICET, Dpto. Bioquímica Clínica, Facultad de Ciencias Químicas, UNC, Córdoba, Argentina A number of physiological and pathological processes produce reactive oxygen species which can promote multiple forms of oxidative injury. Here, we analyzed the chlorpyrifos (CPF) effect on the JEG-3 cell antioxidant defenses. In addition to acetylcholinesterase (AChE) and carboxylesterase (CE) activities, reduced glutathione (GSH) content and the activity of the catalase antioxidant activity (CAT) were measured. Furthermore, hemo-oxygenase 1 (HO-1), and nuclear factor E2-related factor 2 (Nrf2) transcript levels were analyzed. Also, Nrf2 western blot was performed. The results showed that CPF inhibited AChE activity with no changes in CE activity. Alterations in CAT activity and GSH concentration were found. Moreover, CPF increased HO-1 mRNA and Nrf2 at both mRNA and protein levels. The effect on CAT upregulationwas attenuated in N-acetylcysteine-pretreated JEG-3 cells. These studies establish a molecular mechanism for the regulation of CPF detoxification in JEG-3 cells and have implications for controlling the xenobiotics oxidative stress tolerance in trophoblast cell. Supported by CONICET, FONCyT, SECyT-UNC U. N del Comahue, and SACyT ? Beca Carrillo Oñativia ? Ministerio de Salud de la Nación. Keywords: anti-oxidative defense, chlorpyrifos, Nrf2, hemo-oxygenase 1