1-溴丙烷(1-BP) 作为氟利昂等氯氟烃类物质的替代物之一，被广泛应用于工业清洗和作为化工原料中间体用于药品和农药合成。研究表明，1-BP具有神经毒性，可引起工人职业中毒。目前关于1-BP的中毒机制还不是很清楚。本研究拟通过分析1-BP中毒性周围神经病患者和1-BP职业接触工人外周血中P0蛋白抗体的表达以及P0蛋白致敏T淋巴细胞的增殖功能与分泌IFNγ、IL-5、IL-10等细胞因子的水平, 探究P0蛋白引发的自身免疫反应在介导1-BP中毒性周围神经病发生和发展中的作用；并在体外细胞水平分析1-BP引起神经细胞（人神经母细胞瘤细胞SH-SY5Y5和人雪旺细胞hSCs）内氧化损伤水平，以及Nrf2/ARE信号通路调控的抗氧化系统及凋亡相关因子的表达，揭示1-BP引发周围神经病的可能分子机制，为预防和治疗1-BP职业暴露人群健康研究提供科学依据。

1-bromopropane (1-BP), an alternative to ozone-depleting chlorofluorocarbons, has been widely used as a cleaning agent and synthetic intermediate of pharmaceuticals and pesticides。Previous studies have shown that 1-BP has neurotoxicity, can cause occupational poisoning in workers. The mechanism of 1-BP induced neurotoxicity has not been illustrated. In this study, we will analysis the expression of P0 protein in peripheral blood of 1-BP toxic peripheral neuropathy patients and 1-BP occupational exposure workers, detect P0 protein-sensitized T lymphocyte proliferation and secretion of IFNγ, IL-5, IL-10 and other cytokines to investigate the role of P0 protein-induced autoimmune response in the pathogenesis and progression of 1-BP toxic peripheral neuropathy. We also will build up the experimental models with 1-BP–treated SH-SY5Y and hSCs cells in vitro, the levels of oxidative damage in neurons induced by 1-BP and the expression of antioxidant system and apoptosis-related factors regulated by Nrf2 / ARE signaling pathway were analyzed. Revealing the possible molecular mechanism of 1-BP-induced peripheral neuropathy and providing a scientific basis for the prevention and treatment of 1-BP occupational exposure population.