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

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