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Methamidophos induces cytotoxicity and oxidative stress in human peripheral blood mononuclear cells
Author(s) -
RamirezVargas Marco Antonio,
HuertaBeristain Gerardo,
GuzmanGuzman Iris Paola,
AlarconRomero Luz del Carmen,
FloresAlfaro Eugenia,
RojasGarcia Aurora Elizabeth,
MorenoGodinez Ma Elena
Publication year - 2017
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22220
Subject(s) - oxidative stress , malondialdehyde , reactive oxygen species , peripheral blood mononuclear cell , methamidophos , glutathione , chemistry , cytotoxicity , pharmacology , organophosphate , toxicology , biochemistry , biology , pesticide , enzyme , in vitro , agronomy
ABSTRACT Previous studies have shown that organophosphate pesticide (OP) exposure is associated with oxidative stress. Methamidophos (MET) is an OP widely used in agriculture, which is regarded as a highly toxic pesticide and it is a potent inhibitor of acetylcholinesterase. The aim of this study was to evaluate whether MET can induce oxidative stress at low concentrations in primary cultures of human peripheral blood mononuclear cells (PBMCs). PBMCs from healthy individuals were exposed to MET (0–80 mg/L) for 0–72 h. We performed the MTT and neutral‐red assays to assess the cytotoxicity. As indicators of oxidative stress, the levels of reactive oxygen species (ROS) were assessed using flow cytometry, and the malondialdehyde (MDA) and reduced glutathione (GSH) levels were determined. MET decreased the viability of PBMCs in a dose‐dependent manner. At concentrations of 3, 10, or 20 mg/L for 24 h, MET increased the ROS production significantly compared with the vehicle control. Similarly, MET increased the levels of MDA at the same concentrations that increased ROS (10 and 20 mg/L); however, no changes in GSH levels were observed. These results suggest that MET increased the generation of oxidative stress in PBMCs. © 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 147–155, 2017.