共 2 条
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