Assessment of the neurotoxic mechanisms of decabrominated diphenyl ether (PBDE-209) in primary cultured neonatal rat hippocampal neurons includes alterations in second messenger signaling and oxidative stress

被引:65
|
作者
Chen, Jingsi [1 ]
Liufu, Chun [1 ]
Sun, Weiwen [2 ]
Sun, Xiaofang [1 ]
Chen, Dunjin [1 ]
机构
[1] Guangzhou Med Univ, Affiliated Hosp 3, Inst Obstet & Gynecol, Guangzhou 510150, Guangdong, Peoples R China
[2] Guangzhou Med Univ, Affiliated Hosp 2, Inst Neurosci, Guangzhou 510150, Guangdong, Peoples R China
关键词
PBDE-209; Apoptosis; P38; MAPK; Oxidative stress; Calcium ion; DNA methylation; BROMINATED FLAME-RETARDANT; LONG-TERM POTENTIATION; CALCIUM MICRODOMAINS; METHYLATION STATUS; EXPOSURE; MEMORY; CHROMATIN; MICE; ACCUMULATION; ACTIVATION;
D O I
10.1016/j.toxlet.2009.11.020
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
2',2',3',3',4',4',5',5',6',6',-decabrominated diphenyl ether (PBDE-209) is the most widely used polybrominated diphenyl ethers (PBDEs) globally Some animal experiments have found that PBDE-209 caused developmental neurotoxicity. But detailed mechanisms are less well understood Our experiments were conducted to research the potential neurotoxic mechanisms of PBDE-209 in primary cultured neonatal rat hippocampal neurons by measuring cell viability, apoptotic rate, expression of P38 mitogen-activated protein kinases (MAPKs), calcium ion concentration, oxidative stress. nitrous oxide (NO) content. and global gene DNA methylation levels The neurons were exposed to different PBDE-209 concentrations (0, 10, 30 and 50 mu g/ml) file difference between the experimental groups and control groups was significant (P<0 05) PBDE-209 increased the rate of apoptosis, expression of P38 MAPK, calcium ion concentration, reactive oxygen species (ROS) level, malondialdehyde (MDA) content and NO content (P<0 05). In addition, PBDE-209 deceased cell viability, activity Of superoxide dismutase (SOD) and the levels of global gene DNA methylation (P<0 05) The results suggested that PBDE-209 could affect secondary messengers, cause oxidative stress and decrease global gene DNA methylation levels. These actions may contribute to the mechanism of PBDE-209 neurotoxicity (C) 2009 Elsevier Ireland Ltd. All rights reserved
引用
收藏
页码:431 / 439
页数:9
相关论文
共 2 条
  • [1] Effects of Decabrominated Diphenyl Ether (PBDE 209) on Voltage-Gated Sodium Channels in Primary Cultured Rat Hippocampal Neurons
    Xing, Tai-Ran
    Yong, Wu
    Chen, Liang
    Tang, Ming-Liang
    Wang, Ming
    Chen, Ju-Tao
    Ruan, Di-Yun
    ENVIRONMENTAL TOXICOLOGY, 2010, 25 (04) : 400 - 408
  • [2] PBDE-47-induced oxidative stress, DNA damage and apoptosis in primary cultured rat hippocampal neurons
    He, Ping
    He, Weihong
    Wang, Aiguo
    Xia, Tao
    Xu, Bayi
    Zhang, Ming
    Chen, Xuemin
    NEUROTOXICOLOGY, 2008, 29 (01) : 124 - 129