How Chun Ming, Huang Chi-Wei
Department of Bioenvironmental Systems Engineering, National Taiwan University, Taipei 10617, Taiwan.
Department of Marine Environmental Engineering, National Kaohsiung University of Science and Technology, Kaohsiung 81157, Taiwan.
Nanomaterials (Basel). 2023 Jan 10;13(2):289. doi: 10.3390/nano13020289.
The widespread use of zinc oxide nanoparticles (ZnO-NPs) and their release into the environment have raised concerns about the potential toxicity caused by dietary transfer. However, the toxic effects and the mechanisms of dietary transfer of ZnO-NPs have rarely been investigated. We employed the bacteria-feeding nematode as the model organism to investigate the neurotoxicity induced by exposure to ZnO-NPs via trophic transfer. Our results showed that ZnO-NPs accumulated in the intestine of and also in OP50 that they ingested. Additionally, impairment of locomotive behaviors, including decreased body bending and head thrashing frequencies, were observed in that were fed pre-treated with ZnO-NPs, which might have occurred because of damage to the D-type GABAergic motor neurons. However, these toxic effects were not apparent in that were fed pre-treated with zinc chloride (ZnCl). Therefore, ZnO-NPs particulates, rather than released Zn ions, damage the D-type GABAergic motor neurons and adversely affect the locomotive behaviors of via dietary transfer.
氧化锌纳米颗粒（ZnO-NPs）的广泛使用及其向环境中的释放引发了人们对饮食转移所导致潜在毒性的担忧。然而，ZnO-NPs 的毒性效应及饮食转移机制鲜有研究。我们以摄食细菌的线虫作为模式生物，来研究通过营养转移暴露于 ZnO-NPs 所诱导的神经毒性。我们的结果表明，ZnO-NPs 积聚在线虫的肠道以及它们所摄食的 OP50 细菌中。此外，在用 ZnO-NPs 预处理过的 OP50 喂养的线虫中，观察到了运动行为的损伤，包括身体弯曲和头部摆动频率的降低，这可能是由于 D 型γ-氨基丁酸能运动神经元受损所致。然而，在用氯化锌（ZnCl）预处理过的 OP50 喂养的线虫中，这些毒性效应并不明显。因此，ZnO-NPs 颗粒而非释放出的锌离子，会通过饮食转移损伤 D 型γ-氨基丁酸能运动神经元，并对线虫的运动行为产生不利影响。
