Ho I K, Fujimori K, Huang T P, Chang-Tusi H
J Toxicol Environ Health. 1981 Nov-Dec;8(5-6):701-6. doi: 10.1080/15287398109530106.
Plasma and brain levels of chlordecone in chlordecone-induced motor impairment, lethal levels of chlordecone, and cumulative LD50 of chlordecone in the mouse are presented. In terms of biochemical events, the possible contributory role of neurotransmitters in chlordecone-induced neurotoxicity is also discussed. On the basis of the data obtained so far, it is suggested that the dopaminergic pathway and its interaction with other neurotransmitter systems in the basal ganglia may be primarily involved in chlordecone-induced neurotoxicity.
本文介绍了小鼠体内开蓬诱导运动障碍时的血浆和脑内开蓬水平、开蓬致死水平以及开蓬的累积半数致死剂量(LD50)。在生化事件方面,还讨论了神经递质在开蓬诱导的神经毒性中可能的促成作用。根据目前获得的数据,提示多巴胺能通路及其与基底神经节中其他神经递质系统的相互作用可能主要参与了开蓬诱导的神经毒性。