期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 171, 期 1-2, 页码 17-28出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2005.09.007
关键词
15d-PGJ(2); aconitase; methylmercury; MMP (mitochondrial membrane potential); N9 microglia; oxidative stress
Methylmercury (MeHg) causes severe neurological disorders in the central nervous system. This study focused on the effects of MeHg on microglia, macrophage-like cells that reside in the CNS important in neuro-immune interactions. The murine N9 microglial cell line was used in this set of study. MeHg caused reactive oxygen species generation, mitochondrial depolarization and aconitase inactivation, all of which were signs of cellular oxidative stress. MeHg greatly increased microglial IL-6 secretion despite the fact that it severely inhibited protein synthesis. The concentration that caused 50% cell death in 24 h was similar to 9 mu M. Pretreatment of microglia with the prostaglandin derivative, 15-deoxy-delta, 12, 14-Prostaglandin J(2) attenuated MeHg induced cell death. The saving effect did not appear to be mediated through activation of peroxisome proliferator activated receptor (PPAR) since other agonists of these receptors did not prevent MeHg induced microglial death. (c) 2005 Elsevier B.V. All rights reserved.
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