info:eu-repo/semantics/article
Chlorpyrifos inhibits cell proliferation through ERK1/2 phosphorylation in breast cancer cell lines
Fecha
2014-08Registro en:
Ventura, Clara; Venturino, Andres; Miret, Noelia Victoria; Randi, Andrea Silvana; Rivera, Elena Susana; et al.; Chlorpyrifos inhibits cell proliferation through ERK1/2 phosphorylation in breast cancer cell lines; Elsevier; Chemosphere; 120; 8-2014; 343-350
0045-6535
CONICET Digital
CONICET
Autor
Ventura, Clara
Venturino, Andres
Miret, Noelia Victoria
Randi, Andrea Silvana
Rivera, Elena Susana
Nuñez, Mariel
Cocca, Claudia Marcela
Resumen
It is well known the participation of oxidative stress in the induction and development of different pathologies including cancer, diabetes, neurodegeneration and respiratory disorders among others. It has been reported that oxidative stress may be induced by pesticides and it could be the cause of health alteration mediated by pollutants exposure. Large number of registered products containing chlorpyrifos (CPF) is used to control pest worldwide. We have previously reported that 50 μM CPF induces ROS generation and produces cell cycle arrest followed by cell death. The present investigation was designed to identify the pathway involved in CPF-inhibited cell proliferation in MCF-7 and MDA-MB-231 breast cancer cell lines. In addition, we determined if CPF-induced oxidative stress is related to alterations in antioxidant defense system. Finally we studied the molecular mechanisms underlying in the cell proliferation inhibition produced by the pesticide. In this study we demonstrate that CPF (50 μM) induces redox imbalance altering the antioxidant defense system in breast cancer cells. Furthermore, we found that the main mechanism involved in the inhibition of cell proliferation induced by CPF is an increment of p-ERK1/2 levels mediated by H2O2 in breast cancer cells. As PD98059 could not abolish the increment of ROS induced by CPF, we concluded that ERK1/2 phosphorylation is subsequent to ROS production induced by CPF but not the inverse.