Potential threat of Chlorpyrifos to human liver cells via the caspase-dependent mitochondrial pathways

被引:18
作者
Zhang, Yang [1 ]
Chang, Yuansen [1 ]
Cao, Haijing [1 ]
Xu, Wenping [1 ]
Li, Zhong [1 ]
Tao, Liming [1 ]
机构
[1] East China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab Chem Biol, Shanghai 200237, Peoples R China
关键词
Pesticide; Chlorpyrifos; human liver cells; cytotoxic effects; the mitochondrial apoptosis pathway; CYTOCHROME-C RELEASE; OXIDATIVE STRESS; INDUCED APOPTOSIS; IN-VIVO; DEATH; MEMBRANE; BCL-2; BAX; INSECTICIDE; MECHANISMS;
D O I
10.1080/09540105.2017.1373271
中图分类号
O69 [应用化学];
学科分类号
081704 ;
摘要
Chlorpyrifos (CPF) has been widely used around the world as a pesticide for both agricultural and residential application. Although various studies have reported toxicity and health-related effects from CPF exposure, the potential threat and the molecular mechanism of CPF toxicity to human liver have not been well-characterized. In this study, we identify cytotoxicity of CPF to human normal liver cells in vitro. We demonstrate that the viability of QSG7701 cells is inhibited by CPF in a time- and concentration-dependent manner. Intracellular biochemical assays showed that CPF-induced apoptosis of QSG7701 cells concurrent with a decrease in the mitochondrial membrane potential, the release of cytochrome c into the cytosol, up-regulate the expression level of Bax/Bcl-2 and a marked activation of caspase-9/-3. These results indicate that CPF has a potential risk to human liver that can induce apoptosis of human liver cells through caspase-dependent mitochondrial pathways.
引用
收藏
页码:294 / 305
页数:12
相关论文
共 43 条
[1]  
Ahmed M M., 2009, Nature and Science, V7, P49
[2]   Bax is present as a high molecular weight oligomer/complex in the mitochondrial membrane of apoptotic cells [J].
Antonsson, B ;
Montessuit, S ;
Sanchez, B ;
Martinou, JC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (15) :11615-11623
[3]   GENOTOXIC EFFECTS OF THE CARBAMATE INSECTICIDE, METHOMYL .2. IN-VIVO STUDIES WITH PURE COMPOUND AND THE TECHNICAL FORMULATION, LANNATE-25 [J].
BOLOGNESI, C ;
PELUSO, M ;
DEGAN, P ;
RABBONI, R ;
MUNNIA, A ;
ABBONDANDOLO, A .
ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, 1994, 24 (03) :235-242
[4]   Intracellular Bax translocation after transient cerebral ischemia: Implications for a role of the mitochondrial apoptotic signaling pathway in ischemic neuronal death [J].
Cao, GD ;
Minami, M ;
Pei, W ;
Yan, CH ;
Chen, DX ;
O'Horo, C ;
Graham, SH ;
Chen, J .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2001, 21 (04) :321-333
[5]   Rotenone inhibits the mitochondrial permeability transition-induced cell death in U937 and KB cells [J].
Chauvin, C ;
De Oliveira, F ;
Ronot, X ;
Mousseau, M ;
Leverve, X ;
Fontaine, E .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (44) :41394-41398
[6]   MITOCHONDRIAL-MEMBRANE POTENTIAL IN LIVING CELLS [J].
CHEN, LB .
ANNUAL REVIEW OF CELL BIOLOGY, 1988, 4 :155-181
[7]   Mitochondrial dynamics in cell death and neurodegeneration [J].
Cho, Dong-Hyung ;
Nakamura, Tomohiro ;
Lipton, Stuart A. .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2010, 67 (20) :3435-3447
[8]   Apoptosis: A review of programmed cell death [J].
Elmore, Susan .
TOXICOLOGIC PATHOLOGY, 2007, 35 (04) :495-516
[9]  
Evan G, 1997, INT J CANCER, V71, P709, DOI 10.1002/(SICI)1097-0215(19970529)71:5<709::AID-IJC2>3.0.CO
[10]  
2-V