Medical School, Southeast University, Nanjing 210009, China.
Nanjing Institute of Environmental Science, Laboratory of Pesticide Environmental Assessment and Pollution Control, Ministry of Ecology and Environment, Nanjing 210042, China.
NanoImpact. 2022 Apr;26:100403. doi: 10.1016/j.impact.2022.100403. Epub 2022 May 5.
In this study, we determined the roles of oxidative stress and related signals in mediating transgenerational toxicity of 30 nm polystyrene nanoparticles (PS-NPs) in Caenorhabditis elegans. Using brood size and locomotion behavior as endpoints, exposure to 1-100 μg/L PS-NPs caused transgenerational toxicity. Meanwhile, the activation of reactive oxygen species (ROS) was also observed transgenerationally after exposure to 1-100 μg/L PS-NPs. After exposure to 1 μg/L PS-NPs, the transgenerational toxicity was monitored until F2 generation (F2-G) and recovered at F3-G. At the F1-G of 1 μg/L PS-NPs-exposed nematodes, RNAi knockdown of daf-2 with function to inhibit oxidative stress suppressed the transgenerational toxicity and increased the mitochondrial SOD-3 expression. In contrast, at F3-G of 1 μg/L PS-NPs-exposed nematodes, RNAi knockdown of mev-1 with function to induce oxidative stress promoted locomotion and brood size, and suppressed the SOD-3 expression. Moreover, we observed the dynamic expressions of mev-1, daf-2, and sod-2 transgenerationally after exposure to 1 μg/L PS-NPs at P0-G, which further suggested the involvement of MEV-1, DAF-2, and SOD-3 in affecting induction of transgenerational PS-NP toxicity. Therefore, we provided the evidence to suggest the roles of oxidative stress activation and related molecular signals in mediating induction of transgenerational PS-NP toxicity. Our data highlights the crucial function of oxidative stress-related signals during induction of transgenerational PS-NP toxicity.
在这项研究中,我们确定了氧化应激和相关信号在介导 30nm 聚苯乙烯纳米颗粒(PS-NPs)在秀丽隐杆线虫中转代毒性中的作用。使用产卵大小和运动行为作为终点,暴露于 1-100μg/L PS-NPs 会引起转代毒性。同时,暴露于 1-100μg/L PS-NPs 后,也观察到活性氧(ROS)的激活具有跨代效应。在暴露于 1μg/L PS-NPs 后,监测转代毒性直到 F2 代(F2-G),并在 F3-G 时恢复。在暴露于 1μg/L PS-NPs 的线虫的 F1-G 中,具有抑制氧化应激功能的 daf-2 的 RNAi 敲低抑制了转代毒性并增加了线粒体 SOD-3 的表达。相比之下,在暴露于 1μg/L PS-NPs 的线虫的 F3-G 中,具有诱导氧化应激功能的 mev-1 的 RNAi 敲低促进了运动和产卵大小,并抑制了 SOD-3 的表达。此外,我们观察到在暴露于 1μg/L PS-NPs 后,mev-1、daf-2 和 sod-2 的动态表达具有跨代效应,这进一步表明 MEV-1、DAF-2 和 SOD-3 参与影响转代 PS-NP 毒性的诱导。因此,我们提供了证据表明氧化应激激活和相关分子信号在介导转代 PS-NP 毒性的诱导中起作用。我们的数据强调了氧化应激相关信号在诱导转代 PS-NP 毒性中的关键作用。