Zhao Han, Xie Junkai, Wu Shichen, Zhao Xihui, Sánchez Oscar F, Min Sehong, Rochet Jean-Christophe, Freeman Jennifer L, Yuan Chongli
Davidson School of Chemical Engineering, Purdue University, West Lafayette, IN 47907, United States of America.
Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, United States of America.
Sci Total Environ. 2024 Jan 15;908:168307. doi: 10.1016/j.scitotenv.2023.168307. Epub 2023 Nov 8.
Atrazine (ATZ) is one of the most used herbicides in the US and a known endocrine disruptor. ATZ is frequently detected in drinking water, especially in Midwestern regions of the United States, exceeding the EPA regulation of maximum contamination level (MCL) of 3 ppb. Epidemiology studies have suggested an association between ATZ exposure and neurodegeneration. Less, however, is known about the neurotoxic mechanism of ATZ, particularly for exposures at a developmental stage. Here, we exposed floor plate progenitors (FPPs) derived from human induced pluripotent stem cells (hiPSCs) to low concentrations of ATZ at 0.3 and 3 ppb for two days followed by differentiation into dopaminergic (DA) neurons in ATZ-free medium. We then examined the morphology, activity, pathological protein aggregation, and transcriptomic changes of differentiated DA neurons. We observed significant decrease in the complexity of neurite network, increase of neuronal activity, and elevated tau- and α-synuclein (aSyn) pathologies after ATZ exposure. The ATZ-induced neuronal changes observed here align with pathological characteristics in Parkinson's disease (PD). Transcriptomic analysis further corroborates our findings; and collectively provides a strong evidence base that low-concentration ATZ exposure during development can elicit increased risk of neurodegeneration.
阿特拉津(ATZ)是美国使用最广泛的除草剂之一,也是一种已知的内分泌干扰物。在美国的饮用水中经常检测到阿特拉津,尤其是在美国中西部地区,其含量超过了美国环境保护局(EPA)规定的3 ppb的最大污染水平(MCL)。流行病学研究表明,接触阿特拉津与神经退行性变之间存在关联。然而,关于阿特拉津的神经毒性机制,尤其是在发育阶段的接触情况,我们了解得较少。在这里,我们将源自人类诱导多能干细胞(hiPSC)的底板祖细胞(FPP)暴露于0.3和3 ppb的低浓度阿特拉津中两天,然后在无阿特拉津的培养基中分化为多巴胺能(DA)神经元。然后,我们检查了分化后的DA神经元的形态、活性、病理性蛋白质聚集和转录组变化。我们观察到,暴露于阿特拉津后,神经突网络的复杂性显著降低,神经元活性增加,tau蛋白和α-突触核蛋白(aSyn)病变升高。此处观察到的阿特拉津诱导的神经元变化与帕金森病(PD)的病理特征相符。转录组分析进一步证实了我们的发现;并共同提供了有力的证据基础,即发育过程中低浓度阿特拉津暴露会引发神经退行性变风险增加。