CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
artículos
Título:
The organophosphate chlorpyrifos disturbs redox balance and triggers antioxidant defense mechanisms in JEG-3 cells
Autor/es:
CHIAPELLA GRACIELA; FLORES-MARTÍN JÉSICA; RIDANO, MAGALÍ; REYNA LUCIANA; MAGNARELLI DE POTAS GLADIS; PANZETTA DE DUTARI GRACIELA; GENTI DE RAIMONDI SUSANA
Revista:
PLACENTA
Editorial:
W B SAUNDERS CO LTD
Referencias:
Lugar: Londres; Año: 2013 vol. 34 p. 792 - 798
ISSN:
0143-4004
Resumen:
Introduction: Reactive oxygen species (ROS) are produced by a number of physiological and pathological processes which influence the function of a diverse array of cellular events. An imbalance between ROS generation and elimination was reported for different environmental xenobiotics exposure. Here, we analyzed the effect of chlorpyrifos (CPF) on the JEG-3 cell antioxidant defense in conditions where cell viability and morphology were not altered. Methods: Acetylcholinesterase (AChE) activity, reduced glutathione (GSH) content and catalase (CAT) antioxidant enzyme activity were measured by biochemical studies. ROS production was detected using the fluorogenic probe 20,70-dichlorodihydrofluorescein diacetate. The transcript level of superoxide dismutase enzyme 1 (SOD1), glutathione reductase (GR), heme oxygenase-1 (HO-1), and nuclear factor E2- related factor 2 (Nrf2) as well as Nrf2 protein amount were analyzed by quantitative real time PCR and Western blot, respectively. Results: The results showed that CPF inhibited AChE activity, induced ROS production, upregulated CAT activity, and decreased GSH concentration. In response to CPF exposure, GR and HO-1 mRNA levels were increased with no changes in SOD1 mRNA. Furthermore, CPF significantly augmented Nrf2 at both mRNA and protein levels trigging the antioxidant status by increasing nuclear Nrf2 translocation. Discussion and conclusion: Taken together, these data indicate that JEG-3 cells are able to attenuate the oxidative stress induced by CPF through the adaptive activation of the Nrf2/ARE pathway.