摘要
三氯乙烯(TCE)是一种常用工业溶剂,具有高度挥发性和脂溶性,广泛存在于环境中。近期流行病学证据表明,接触TCE可能导致帕金森病(PD)。其机制与抑制线粒体酶活性、氧化应激、炎性反应途径和诱导α-synuclein聚集引起黑质纹状体多巴胺能神经元损伤相关。TCE下游代谢物三氯乙醛可在体内与色胺结合产生1-甲基-4-苯基1,2,3,6-四氢吡啶(MPTP)类似物1-三氯甲基-1,2,3,4-四氢化-β-咔啉(TaClo)特异性抑制线粒体复合体Ⅰ导致多巴胺能神经元受损。本文就TCE的一般性质、体内代谢过程、与PD发病的关系、可能机制、目前研究中的问题进行总结和展望。
Trichloroethylene（TCE） is a widely-used industry solvent which has strong volatility and solubility and is ubiquitous in the environment. The epidemiology evidence showed that ever exposure to TCE may be associated with significantly increased risk of Parkinson＇ s disease （PD）. TCE can selectively cause dopaminergic neurodegeneration, which may be mediated by mitochondrial dysfunction, inflammation, oxidative stress and gathering of o^-synuclein. In the mean time, trichloroacetaldehyde, one of the metabolites of TCE, can be combined with tryptamine in human body. The reaction forms a new chemical substance, 1-trichloromethyl-1, 2, 3, 4-tetrvahydro-13-carboline（TaClo）, which is similar with MPTP in structure. TaClo has the ability to inhibit mitochondria complex 1 and cause damage to dopaminergic neurons. In summary, TCE may have strong relationship with the development of PD and the mechanism is still under exploration.
出处
《中国临床神经科学》
2013年第2期182-187,共6页
Chinese Journal of Clinical Neurosciences
