Nano-plastics and gastric health: Decoding the cytotoxic mechanisms of polystyrene nano-plastics size

文献类型： 外文期刊

第一作者： Jiang, Qichen

作者： Jiang, Qichen;Qin, Wei;Han, Mingming;Zhu, Tian;Liang, Ji;Zhu, Chenxi;Abdullah, Anisah Lee Binti;Rubinstein, James;Wang, Hong;Worthington, Richard;George, Andrew;Li, Yiming

作者机构：

关键词： Nano-plastics size; Gastric health; Cellular death; Mitochondrial membrane potential; Calcium channel

期刊名称：ENVIRONMENT INTERNATIONAL （ 影响因子：11.8； 五年影响因子：12.4 ）

ISSN： 0160-4120

年卷期： 2024 年 183 卷

页码：

收录情况： SCI

摘要： Gastrointestinal diseases exert a profound impact on global health, leading to millions of healthcare interventions and a significant number of fatalities annually. This, coupled with escalating healthcare expenditures, underscores the need for identifying and addressing potential exacerbating factors. One emerging concern is the pervasive presence of microplastics and nano-plastics in the environment, largely attributed to the indiscriminate usage of disposable plastic items. These nano-plastics, having infiltrated our food chain, pose a potential threat to gastrointestinal health. To understand this better, we co-cultured human gastric fibroblasts (HGF) with polystyrene nano-plastics (PS-NPs) of diverse sizes (80, 500, 650 nm) and meticulously investigated their cellular responses over a 24-hour period. Our findings revealed PS particles were ingested by the cells, with a notable increase in ingestion as the particle size decreased. The cellular death induced by these PS particles, encompassing both apoptosis and necrosis, showcased a clear dependence on both the particle size and its concentration. Notably, the larger PS particles manifested more potent cytotoxic effects. Further analysis indicated a concerning reduction in cellular membrane potential, alongside a marked increase in ROS levels upon PS particles exposure. This suggests a significant disruption of mitochondrial function and heightened oxidative stress. The larger PS particles were especially detrimental in causing mitochondrial dysfunction. In-depth exploration into the PS particles impact on genes linked with the permeability transition pore (PTP) elucidated that these PS particles instigated an internal calcium rush. This surge led to a compromise in the mitochondrial membrane potential, which in tandem with raised ROS levels, further catalyzed DNA damage and initiated cell death pathways. In essence, this study unveils the intricate mechanisms underpinning cell death caused by PS particles in gastric epithelial cells and highlighting the implications of PS particles on gastrointestinal health. The revelations from this research bear significant potential to shape future healthcare strategies and inform pertinent environmental policies.

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