Polybrominated Diphenyl Ethers Quinone Induced Parthanatos-like Cell Death through a Reactive Oxygen Species-Associated Poly(ADP-ribose) Polymerase 1 Signaling

被引：19

作者：

Dong, Wenjing ^{[1
]}

Yang, Bingwei ^{[1
]}

Wang, Yawen ^{[1
]}

Yuan, Jia ^{[1
]}

Fan, Yunqi ^{[1
]}

Song, Erqun ^{[1
]}

Song, Yang ^{[1
]}

机构：

[1] Southwest Univ, Coll Pharmaceut Sci, Minist Educ, Key Lab Luminescence & Real Time Analyt Chem, Chongqing 400715, Peoples R China

来源：

CHEMICAL RESEARCH IN TOXICOLOGY | 2018年 / 31卷 / 11期

基金：

中国国家自然科学基金;

关键词：

OXIDATIVE DNA-DAMAGE; INDUCED GENOTOXICITY; ADDUCT FORMATION; PBDES; METABOLISM; APOPTOSIS; STRESS; RESPONSES; PROMOTES; DUST;

D O I：

10.1021/acs.chemrestox.8b00168

中图分类号：

R914 [药物化学];

学科分类号：

100701 ;

摘要：

Polybrominated diphenyl ethers (PBDEs) are emerging organic environmental pollutants, which were accused of various toxic effects. Here, we studied the role of a potential PBDEs quinone metabolite, PBDEQ on cytotoxicity, oxidative DNA damage, and the alterations of signal cascade in HeLa cells. PBDEQexposure leads to reactive oxygen species (ROS) accumulation, mitochondrial membrane potential (MMP) loss, lactate dehydrogenase (LDH) release, increasing terminal transferase-mediated dUTP-biotin nick end labeling (TUNEL) positive foci, and the elevation of apoptosis rate. Furthermore, we showed PBDEQ exposure result in increased DNA migration, micronucleus frequency, and the promotion of 8-OHdG and phosphorylation of histone H2AX (gamma-H2AX) levels. Mechanism study indicated that PBDEQ caused poly(ADP-ribose) polymerase 1 (PARP-1) activation and apoptosis-inducing factor (AIF) nuclear translocation. All together, these results confirmed the occurrence of parthanatos-like cell death upon PBDEQ exposure.

引用

页码：1164 / 1171

页数：8

共 37 条

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