The environmental pollutant BDE-209 regulates NO/cGMP signaling through activation of NMDA receptors in neurons
The environmental pollutant BDE-209 regulates NO/cGMP signaling through activation of NMDA receptors in neurons
复制标题
环境污染物 BDE-209 通过激活神经元中的 NMDA 受体来调节 NO/cGMP 信号传导。
DOI：
10.1007/s11356-017-0651-5
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发表时间：
2018-02-01
影响因子：
5.8
通讯作者：
Chen, Dunjin
中科院分区：
文献类型：
--
作者：
Chen, Jingsi;Li, Xiuying;Chen, Dunjin
The common flame retardant decabrominated diphenyl ether (BDE-209) is a persistent organic pollutant. Epidemiological studies have revealed that prenatal or postnatal exposure to BDE-209 can result in delayed cognitive development, and BDE-209 has been shown to be toxic to cultured neurons with maturation interference effects. However, its neurotoxic mechanism remains unclear. Nitric oxide/cyclic guanosine monophosphate (NO/cGMP) signaling plays an important role in regulating neuronal maturation. We examined the influence of BDE-209 (100, 200, and 400 nM) on NO production and cGMP levels signaling in rodent neurons in vitro, with or without pretreatment N-methyl-D-aspartate (NMDA) receptor antagonism. We found that nanomolar concentrations of BDE-209 affected levels of the second messengers NO and cGMP, and that these effects could be blocked by NMDA receptor antagonism. Moreover, BDE-209 activation of NMDA receptors inhibited the expression of phosphodiesterases (PDEs), which modulate intracellular cGMP levels, and increased the Bcl-2/Bax ratio, favoring apoptosis induction. Our studies implicate the NMDA-NO/cGMP pathway in the pathogenic mechanism through which BDE-209 induces neurotoxicity.
