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 |
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Authors: | Jingsi Chen Chun Liufu Weiwen Sun Xiaofang Sun Dunjin Chen |
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Affiliation: | 1. The Third Affiliated Hospital of Guangzhou Medical College, Institute of Gynecology and Obstetrics, Guangzhou, China;2. The Second Affiliated Hospital of Guangzhou Medical College, Institute of Neuroscience, Guangzhou, China |
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Abstract: | 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 μg/ml). The 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. |
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Keywords: | PBDE-209 Apoptosis P38 MAPK Oxidative stress Calcium ion DNA methylation |
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