School of Freshwater Sciences, University of Wisconsin-Milwaukee, 600 E. Greenfield Avenue, Milwaukee, WI, 53204, USA; Zoology Department, Faculty of Science, Damietta University, New Damietta 34511, Damietta, Egypt.
Zoology Department, Faculty of Science, Damietta University, New Damietta 34511, Damietta, Egypt.
Environ Pollut. 2018 Nov;242(Pt A):433-448. doi: 10.1016/j.envpol.2018.06.030. Epub 2018 Jun 12.
Exposure to ZnO-nanoparticles (NPs) in embryonic zebrafish reduces hatching rates which can be mitigated with dissolved organic material (DOM). Although hatching rate can be a reliable indicator of toxicity and DOM mitigation potential, a fish that has been exposed to ZnO-NPs or any other toxicant may also exhibit other abnormal phenotypes not readily detected by the unaided eye. In this study, we moved beyond hatching rate analysis to investigate the consequences of ZnO-NPs exposure on the nervous and vascular systems in developing zebrafish. Zebrafish exposed to ZnO-NPs (1-100 ppm) exhibited an array of cellular phenotypes including: abnormal secondary motoneuron (SMN) axonal projections, abnormal dorsal root ganglion development and abnormal blood vessel development. Dissolved Zn (<10 kDa) exposure also caused abnormal SMN axonal projections, but to a lesser extent than ZnO-NPs. The ZnO-NPs-induced abnormal phenotypes were reversed in embryos concurrently exposed with various types of DOM. In these acute mitigation exposure experiments, humic acid and carbohydrate, along with natural organic matter obtained from the Suwannee River in Georgia and Milwaukee River in Wisconsin, were the best mitigators of ZnO-NPs-induced motoneuron toxicity at 96 h post fertilization. Further experiments were performed to determine if the ZnO-NPs-induced, abnormal axonal phenotypes and the DOM mitigated axonal phenotypes could persist across generations. Abnormal SMN axon phenotypes caused by ZnO-NPs-exposure were detected in F1 and F2 generations. These are fish that have not been directly exposed to ZnO-NPs. Fish mitigated with DOM during the acute exposure (F0 generation) had a reduction in abnormal motoneuron axon errors in larvae of subsequent generations. Therefore, ZnO-NPs exposure results in neurotoxicity in developing zebrafish which can persist from one generation to the next. Mitigation with DOM can reverse the abnormal phenotypes in an acute embryonic exposure context, as well as across generations, resulting in healthy fish.
胚胎斑马鱼暴露于氧化锌纳米颗粒（NPs）会降低孵化率，而溶解有机物（DOM）可以减轻这种影响。虽然孵化率可以作为毒性和 DOM 缓解潜力的可靠指标，但暴露于氧化锌 NPs 或任何其他有毒物质的鱼类也可能表现出其他肉眼不易察觉的异常表型。在这项研究中，我们超越了孵化率分析，研究了氧化锌 NPs 暴露对发育中斑马鱼的神经系统和血管系统的影响。暴露于氧化锌 NPs（1-100ppm）的斑马鱼表现出一系列细胞表型，包括：异常的次级运动神经元（SMN）轴突投射、异常的背根神经节发育和异常的血管发育。溶解的 Zn（<10kDa）暴露也会导致 SMN 轴突投射异常，但程度低于 ZnO-NPs。在同时暴露于各种类型 DOM 的胚胎中，氧化锌 NPs 诱导的异常表型得到了逆转。在这些急性缓解暴露实验中，腐殖酸和碳水化合物，以及来自佐治亚州苏万尼河和威斯康星州密尔沃基河的天然有机物，是在受精后 96 小时缓解氧化锌 NPs 诱导的运动神经元毒性的最佳缓解剂。进一步的实验旨在确定 ZnO-NPs 诱导的异常轴突表型和 DOM 缓解的轴突表型是否可以在代际间持续存在。在 F1 和 F2 代中检测到由 ZnO-NPs 暴露引起的异常 SMN 轴突表型。这些鱼类没有直接暴露于 ZnO-NPs。在急性暴露期间（F0 代）用 DOM 缓解的鱼类在后代幼虫中的异常运动神经元轴突错误减少。因此，氧化锌 NPs 暴露会导致发育中的斑马鱼产生神经毒性，这种毒性可以从一代传递到下一代。在急性胚胎暴露的情况下，DOM 的缓解可以逆转异常表型，并且可以在代际间持续存在，从而产生健康的鱼类。
