Alteration in mitochondrial function and glutamate metabolism affected by 2-chloroethanol in primary cultured astrocytes
Alteration in mitochondrial function and glutamate metabolism affected by 2-chloroethanol in primary cultured astrocytes
复制标题
原代培养星形胶质细胞中2-氯乙醇影响线粒体功能和谷氨酸代谢的改变
DOI：
10.1016/j.tiv.2016.09.005
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发表时间：
2016
影响因子：
3.2
通讯作者：
Jin Yaping
中科院分区：
文献类型：
--
作者：
Sun Qi;Liao Yingjun;Wang Tong;Wang Gaoyang;Zhao Fenghong;Jin Yaping
The aim of this study was to explore the mechanisms that contribute to 1,2-dichloroethane (1,2-DCE) induced brain edema by focusing on alteration of mitochondrial function and glutamate metabolism in primary cultured astrocytes induced by 2-chloroethanol (2-CE), a metabolite of 1,2-DCE in vivo. The cells were exposed to different levels of 2-CE in the media for 24 h. Mitochondrial function was evaluated by its membrane potential and intracellular contents of ATP, lactic acid and reactive oxygen species (ROS). Glutamate metabolism was indicated by expression of glutamine synthase (GS), glutamate–aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) at both protein and gene levels. Compared to the control group, exposure to 2-CE could cause a dose dependent damage in astrocytes, indicated by decreased cell viability and morphological changes, and supported by decreased levels of nonprotein sulfhydryl (NPSH) and inhibited activities of Na+/K+-ATPase and Ca2 +-ATPase in the cells. The present study also revealed both mitochondrial function and glutamate metabolism in astrocytes were significantly disturbed by 2-CE. Of which, mitochondrial function was much vulnerable to the effects of 2-CE. In conclusion, our findings suggested that mitochondrial dysfunction and glutamate metabolism disorder could contribute to 2-CE-induced cytotoxicity in astrocytes, which might be related to 1,2-DCE-induced brain edema.
