摘要
慢性锰暴露可能引起多巴胺能功能选择性障碍、谷氨酸能运输系统受损、活性氧产生、"外周型"苯二氮卓类受体结合位点增加、参与糖分解的三磷酸甘油醛脱氢酶及其它酶类代谢异常,导致能量代谢变化、细胞形态改变、神经元损伤及细胞外谷氨酸浓度增加,这对于从病理生理学角度阐明锰神经毒性机制具有十分重要的作用。
Chronic exposure to manganese causes selective dopaminergic dysfunction,impairment of glutamate transport,production of active oxygen,increased densities of binding sites for the ＂peripheral-type＂ benzodiazepine receptor,alterations of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase and abnormal metabolism of other enzymes.Such effects can lead to changed energy metabolism,altered cellular morphology,damaged neurons and increased extracellular glutamate concentration.It plays a very important role to clarify the pathophysiologic mechanism of manganese neuroxicity.
出处
《铁道劳动安全卫生与环保》
2009年第6期292-295,共4页
Railway Occupational Safety Health & Environmental Protection
基金
国家自然科学基金项目(30760210)
广西自然科学基金(0991129)
广西教育厅研究生教育创新计划(2008105981004D32)
关键词
锰
神经毒性
病理生理学
manganese
neurotoxicity
pathophysiology
