Chlorpyrifos induces reticulum endoplasmic stress in JEG-3 cells

L. REYNA; ME. RIDANO; JB. FLORES-MARTÍN; GM. PANZETTA DE DUTARI; S GENTI DE RAIMONDI

Simposio; VI Latin American Symposium on Maternal-Fetal Interaction and Placenta (SLIMP) and the V Latin American Symposium on Reproductive Immunology (LASRI); 2015

SLIMP LASRI

Chlorpyrifos (CPF) is an organophosphorous pesticide widely used inagricultural, industrial, and household applications. We have previouslyshown that JEG-3 cells are able to attenuate the oxidative stress induced byCPF through the adaptive activation of the Nrf2/ARE pathway. Particularly,we found that cells treated with 50 ìM or 100 ìM CPF lead to an early Nrf2increase at both mRNA and protein levels, triggering the antioxidant statusand nuclear Nrf2 translocation.Objectives: This work was performed to evaluate whether CPF inducesreticulum endoplasmic (ER) stress in JEG-3 cells.Methods: Cells were exposed to 50 ìM or 100 ìM CPF for 3 or 24 h inconditions where cell viability was not altered. Western blot assays wereused to explore the protein levels of ER stress biomarkers.Results: In response to CPF the ER stress biomarker proteins glucoseregulatedprotein 78 and calnexin were significantly augmented at 24 h oftreatment, whereas protein disulfide isomerase showed an increasingtrend although statistically non-significant. Furthermore, CPF also activatedinositol-requiring enzyme 1, a sensor for the unfolded proteinresponse. Since reported studies indicate that p53 plays a critical role inthe cellular response to ER stress, the effect of CPF was investigated bymeasuring p53 protein expression. The data indicate that CPF induces anearly p53 expression at 3 h of CPF cell exposure whichwas recovered to thebasal value at 24 h of CPF treatment.Conclusions: Altogether, these findings indicate that CPF induces ER stressin JEG-3 cells; however they are able to trigger an adaptive protectionresponse against the xenobiotic injury.Supported by CONICET, FONCyT and SECyT-UNC