鱼藤酮对多巴胺能神经元的损伤作用及机制

鱼藤酮等环境毒物的长期接触可能与帕金森病发病有关。鱼藤酮(Rotenone)是线粒体复合酶Ⅰ抑制剂，可以抑制多巴胺能神经元线粒体复合酶Ⅰ的活性、降低线粒体膜电位、诱导细胞内活性氧的产生，从而导致多巴胺能神经元α-突触核蛋白(α-synuclein)表达增加、路易小体(Lewy bodies)形成，DJ-1和Parkin的突变以及细胞微管破坏。

Mechanisms of rotenone-induced dopaminergic neurons injury

Parkinson’s disease (PD) is a late-onset progressive neurodegenerative disorder. The etiology of PD is not completely understood, but it is believed that the inhibition of the mitochondrial complex Ⅰ, such as rotenone may increase PD risk. Indeed many of the processes which have been suggested to be involved in its mechanisms include impairment of the mitochondrial electron transfer chain，reduction of the mitochondrial membrane potential (ΔΨm) and increasing oxidative stress. The mitochondrial complexⅠinhibition may be the central cause of sporadic PD and derangements in complexⅠ cause α-synuclein aggregation and the formation of Lewy bodies; mutation of parkin and DJ-1 and the dysfunction of microtubule.