Shanghai Key Laboratory of Atmospheric Particle Pollution and Prevention (LAP(3)), Fudan Tyndall Center, Department of Environmental Science and Engineering, Fudan University, Shanghai 200433, China.
Shanghai Key Laboratory of Atmospheric Particle Pollution and Prevention (LAP(3)), Fudan Tyndall Center, Department of Environmental Science and Engineering, Fudan University, Shanghai 200433, China.
Water Res. 2022 Sep 1;223:118960. doi: 10.1016/j.watres.2022.118960. Epub 2022 Aug 7.
Nanoplastics, as emerging contaminants, may be degraded from microplastics and released into aquatic systems globally, which pose threats to human health via ingestion with food or water. Although plastic fragments have been isolated from placental tissues in pregnant women, little is known about the direct toxicity of nanoplastics on human placental cells that plays a critical role in maintaining healthy growth of fetus. This study explored the mechanistic toxicity of polystyrene nanoplastics (PS-NPs) with different sizes (25, 50, 100 and 500 nm) and surface charges (-NH, -COOH and unlabeled) on human placental cells. Results showed that PS-NPs had size- and surface charge-specific toxicity pattern. The smaller the PS-NP size was, the greater the toxicity induced on human placental cells. In terms of surface charges, NH-labeled PS-NPs caused greater effects on cytotoxicity, inhibition of protein kinase A (PKA) activity, oxidative stress, and cell cycle arrest compared to COOH-labeled and unmodified PS-NPs. PS-NPs also induced size- and surface charge-dependent expression profiles of genes involved in various and interrelated toxicity pathways. In particular, PS-NPs increased intracellular reactive oxygen species in human placental cells, which can induce DNA damage and lead to cell cycle arrest in G1or G2 phase, inflammation and apoptosis. Our findings provide empirical evidences that the negative effects of nanoplastics on human placental cells, and highlight the necessity to conduct risk assessment of nanoplastics on female reproduction and fetal development.
纳米塑料作为新兴污染物,可能会从微塑料中降解并释放到全球水生系统中,通过食物或水摄入会对人类健康构成威胁。虽然已经从孕妇的胎盘组织中分离出了塑料碎片,但对于纳米塑料对在维持胎儿健康生长方面起着关键作用的人胎盘细胞的直接毒性知之甚少。本研究探讨了不同尺寸(25、50、100 和 500nm)和表面电荷(-NH、-COOH 和未标记)的聚苯乙烯纳米塑料(PS-NPs)对人胎盘细胞的机制毒性。结果表明,PS-NPs 具有尺寸和表面电荷特异性毒性模式。PS-NP 的尺寸越小,对人胎盘细胞的毒性越大。就表面电荷而言,与 COOH 标记和未修饰的 PS-NPs 相比,NH 标记的 PS-NPs 对细胞毒性、蛋白激酶 A(PKA)活性抑制、氧化应激和细胞周期停滞的影响更大。PS-NPs 还诱导了与各种相互关联的毒性途径相关的基因的大小和表面电荷依赖性表达谱。特别是,PS-NPs 增加了人胎盘细胞内的活性氧,这可能导致 DNA 损伤,并导致 G1 或 G2 期细胞周期停滞、炎症和细胞凋亡。我们的研究结果提供了纳米塑料对人胎盘细胞的负面影响的经验证据,并强调了有必要对纳米塑料对女性生殖和胎儿发育的风险进行评估。