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聚苯乙烯微纳米颗粒诱导正常结肠细胞代谢重编程:人类健康的风险因素。

Polystyrene micro and nano-particles induce metabolic rewiring in normal human colon cells: A risk factor for human health.

机构信息

ISBE. IT/ Centre of Systems Biology, Piazza Della Scienza 4, 20126, Milan, Italy; Department of Biotechnology and Biosciences, University of Milano-Bicocca, Piazza Della Scienza 2, 20126, Milan, Italy.

ISBE. IT/ Centre of Systems Biology, Piazza Della Scienza 4, 20126, Milan, Italy; Institute of Molecular Bioimaging and Physiology (IBFM), National Research Council (CNR), Segrate, MI, Italy.

出版信息

Chemosphere. 2022 Sep;303(Pt 1):134947. doi: 10.1016/j.chemosphere.2022.134947. Epub 2022 May 14.

Abstract

Polystyrene is a thermoplastic polymer widely used in commercial products. Like all plastics, polystyrene can be degraded into microplastic and nanoplastic particles and ingested via food chain contamination. Although the ecological impact due to plastic contamination is well known, there are no studies indicating a carcinogenic potential of polystyrene microplastics (MPs) and nanoplastics (NPs). Here, we evaluated the effects of the MPs and NPs on normal human intestinal CCD-18Co cells. Our results show that internalization of NPs and MPs induces metabolic changes under both acute and chronic exposure by inducing oxidative stress, increasing glycolysis via lactate to sustain energy metabolism and glutamine metabolism to sustain anabolic processes. We also show that this decoupling of nutrients mirrors the effect of the potent carcinogenic agent azoxymethane and HCT15 colon cancer cells, carrying out the typical strategy of cancer cells to optimize nutrients utilization and allowing metabolic adaptation to environmental stress conditions. Taken together our data provide new evidence that chronic NPs and MPs exposure could act as cancer risk factor for human health.

摘要

聚苯乙烯是一种广泛应用于商业产品的热塑性聚合物。与所有塑料一样,聚苯乙烯会降解成微塑料和纳米塑料颗粒,并通过食物链污染被摄入。尽管塑料污染对生态环境的影响众所周知,但目前尚无研究表明聚苯乙烯微塑料(MPs)和纳米塑料(NPs)具有致癌潜力。在这里,我们评估了 MPs 和 NPs 对正常人类肠道 CCD-18Co 细胞的影响。我们的结果表明,无论是在急性暴露还是慢性暴露下,NPs 和 MPs 的内化都会通过诱导氧化应激、通过乳酸增加糖酵解以维持能量代谢以及通过谷氨酰胺代谢维持合成代谢过程,引起代谢变化。我们还表明,这种营养物质的解偶联反映了强致癌剂偶氮甲烷和 HCT15 结肠癌细胞的作用,执行了癌细胞的典型策略,即优化营养物质的利用,并允许代谢适应环境应激条件。总之,我们的数据提供了新的证据,表明慢性 NPs 和 MPs 暴露可能成为人类健康的致癌因素。

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