Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, School of Life Sciences, Lanzhou University, China; Department of Marine Ecology, College of Marine Life Sciences, Ocean University of China, Qingdao 266003, China.
Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, School of Life Sciences, Lanzhou University, China.
Sci Total Environ. 2024 Apr 1;919:170790. doi: 10.1016/j.scitotenv.2024.170790. Epub 2024 Feb 7.
The combined pollution of lead (Pb) and polystyrene microplastics (PS-MPs) is common in aquatic environments. However, the combined neurotoxicity of these two pollutants is still poorly understood. In this study, zebrafish (Danio rerio) larvae were used to assess the combined neurotoxicity and mechanism of Pb and PS-MPs at environmentally relevant concentrations. The results showed that Pb (10 μg/L) induced abnormal behavior including significantly reduced movement distance, maximum acceleration, and average velocity (P < 0.05) along with altered expression of neurodevelopment-related genes (gap43 and α1-tubulin) (P < 0.05). PS-MPs (25 μg/L, 250 μg/L; diameter at 25 μm) co-exposure not only significantly reduced the concentration of Pb in the exposed solution (P < 0.01), but also decreased the uptake of Pb by downregulating the divalent metal transporter 1 gene (dmt1) (P < 0.01), thereby alleviating Pb-induced neurotoxicity. However, to demonstrate that PS-MPs alleviate the neurotoxicity of Pb by reducing Pb uptake, upregulation of dmt1 by addition of deferoxamine (DFO, an efficient iron chelator, 100 μM) significantly increased the Pb uptake and exacerbated neurotoxicity in zebrafish. In summary, our results demonstrated that PS-MPs alleviate Pb neurotoxicity by downregulating the mRNA level of dmt1 and decreasing the Pb uptake. This study provides a new insight into the combined neurotoxicity and underlying mechanisms of PS-MPs and Pb on zebrafish.
铅(Pb)和聚苯乙烯微塑料(PS-MPs)的联合污染在水生环境中很常见。然而,这两种污染物的联合神经毒性仍知之甚少。在这项研究中,使用斑马鱼(Danio rerio)幼虫来评估这两种污染物在环境相关浓度下的联合神经毒性及其机制。结果表明,Pb(10μg/L)诱导了异常行为,包括运动距离、最大加速度和平均速度明显减少(P<0.05),同时神经发育相关基因(gap43 和α1-微管蛋白)的表达也发生改变(P<0.05)。PS-MPs(25μg/L、250μg/L;直径为 25μm)共暴露不仅显著降低了暴露溶液中 Pb 的浓度(P<0.01),而且通过下调二价金属转运蛋白 1 基因(dmt1)来减少 Pb 的摄取,从而减轻 Pb 诱导的神经毒性(P<0.01)。然而,为了证明 PS-MPs 通过减少 Pb 的摄取来减轻 Pb 的神经毒性,通过添加去铁胺(DFO,一种有效的铁螯合剂,100μM)上调 dmt1 显著增加了 Pb 的摄取,并加剧了斑马鱼的神经毒性。总之,我们的结果表明 PS-MPs 通过下调 dmt1 的 mRNA 水平和减少 Pb 的摄取来减轻 Pb 的神经毒性。本研究为 PS-MPs 和 Pb 对斑马鱼的联合神经毒性及其潜在机制提供了新的见解。