摘要
机体过量的锰暴露会导致进行性神经变性损害,严重者可出现帕金森氏病样症状。锰对线粒体有特殊的亲和力,过量的锰蓄积在线粒体,会引起线粒体形态发生改变。锰可通过阻断线粒体能量转换、诱导线粒体基因组突变和提高自由基产量而干扰线粒体的功能,最终导致ATP产生减少,影响细胞呼吸。因此,探讨锰的线粒体毒性将有助于进一步阐明锰神经毒作用机制,对锰中毒和帕金森氏病的预防和治疗也具有十分重要的意义。
Overexposure to manganese can lead to progressive, resulting in syndromes similar to idiopathic Parkinson＇ s disease. Mn permanent, neurodegenerative damage accumulates specifically in mitochondrial matrix. Excessive manganese cumulates in mitochondria which will change mitochondrial structure. Manganese might disrupt mitochondrial function by inhibition of energy transduction, the induction of mutations of the mitochondrial genome and through the enhanced generation of free radicals, eventually decreasing the generation of ATP and influencing cells＇ breath. Therefor, it has very important to probe the mitochondrial toxicity of manganese further for protecting and treating Mn toxicity and Parkinson＇ s disease.
出处
《铁道劳动安全卫生与环保》
2005年第6期297-300,共4页
Railway Occupational Safety Health & Environmental Protection
关键词
锰
线粒体
毒性
manganese
mitochondrial
toxicity
