化学
镉
细胞毒性
毒性
细胞内
生物物理学
生物利用度
纳米毒理学
氧化应激
细胞生物学
细胞毒性T细胞
氧化损伤
金属
细胞凋亡
内吞作用
环境毒理学
线粒体
金属硫蛋白
微塑料
平衡
镉暴露
金属毒性
DNA损伤
生物化学
氧化磷酸化
杀伤力
多核
拉明
持久性(不连续性)
作者
X. Y. Wang,Shuqi Guo,Xiangxiang Li,Xingchen Zhao,Shaoyang Hu,Rutao Liu
标识
DOI:10.1021/acs.est.5c12515
摘要
Nanoplastics are generally regarded as exacerbating heavy metal toxicity by acting as Trojan horse carriers of metal ions. Here, we demonstrate that aged polystyrene nanoplastics (PS-NPs) unexpectedly mitigate cadmium [Cd(II)]-induced acute cytotoxicity in osteoblasts, suggesting a modulatory role beyond passive transport. Aged PS-NPs effectively adsorb Cd(II) via electrostatic and coordination interactions, forming larger aggregates that significantly limit cellular uptake compared to free Cd(II). This mitigating effect was further associated with restricted Cd(II) release, altered subcellular trafficking, and limited mitochondrial penetration, as revealed by super-resolution structured illumination microscopy (SIM). In addition, molecular-level analyses demonstrated that aged PS-NPs impaired Cd(II) binding to biomolecules. Collectively, these mechanisms reduced Cd(II) bioavailability. Quantitatively, aged PS-NPs reduced intracellular free Cd(II) by ∼14-29% and attenuated cytotoxic responses by ∼15-33% with respect to oxidative stress, membrane damage, and apoptosis during 24 h of acute co-exposure. Our findings reveal an unexpected mitigating role of aged nanoplastics in metal toxicity, challenging their conventional view as merely passive carriers. However, given the environmental persistence of both nanoplastics and Cd(II), their long-term co-exposure risks warrant urgent assessment.
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