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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。
Trichlorethylene (TCE) is a common industrial solvent, highly volatile and fat soluble, widely present in the environment. Recent epidemiological evidence suggests that exposure to TCE may lead to Parkinson’s disease (PD). Its mechanism is related to the inhibition of mitochondrial enzyme activity, oxidative stress, inflammatory response pathways and the induction of α-synuclein aggregation resulting in nigrostriatal dopaminergic neuron damage. TCE downstream metabolite chloral may combine with tryptamine in vivo to produce 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine (MPTP) analog 1-trichloromethyl- Specific inhibition of mitochondrial complex I by 2,3,4-tetrahydro-β-carboline (TaClo) results in impaired dopaminergic neurons. In this paper, the general nature of TCE, metabolic processes in vivo, the relationship with the pathogenesis of PD, possible mechanisms, the problems in the current study are summarized and prospects.