4.7 Article

Distinct accumulation of nanoplastics in human intestinal organoids

期刊

SCIENCE OF THE TOTAL ENVIRONMENT
卷 838, 期 -, 页码 -

出版社

ELSEVIER
DOI: 10.1016/j.scitotenv.2022.155811

关键词

Nanoplastics; Toxicology; Human intestinal organoids; Accumulation; Endocytosis

资金

  1. National Natural Science Foundation of China [11972099]
  2. Venture & Innovation Support Program for Chongqing Overseas Returnees [cx2020079]
  3. Scientific and Technological Innovation Project of Chengdu-Chongqing Area Double-city Economic Circle Construction [KJCXZD2020007]

向作者/读者索取更多资源

This study investigates the accumulation, toxicity, and mechanism of polystyrene nanoplastics (PS-NPs) in human intestinal cells. The results show that PS-NPs can accumulate in different types of intestinal cells, leading to cell apoptosis and inflammatory response. The inhibition of clathrin-mediated endocytosis effectively reduces the accumulation of PS-NPs in secretive cells. This research not only reveals the potential uptake and toxicity of PS-NPs in human intestines, but also proposes a therapeutic approach to alleviate their toxicity through endocytosis inhibition.
Plastic particles, especially nanoplastics, represent an emerging concern of threat to human health, oral uptake is an important pathway for the plastic particles ingestion by human. While their fate and adverse effects in animal gastrointestinal tract are increasingly investigated, knowledge about their uptake and toxicity in human intestine is still limited. Here, by exposing human intestinal organoids to polystyrene nanoplastics (PS-NPs, similar to 50 nm in size) with concentrations of 10 and 100 mu g/mL, we present evidence of their distinct accumulation in various type cells in intestinal organoids, then causing the cell apoptosis and inflammatory response. Our results further revealed that the effective inhibition of PS-NPs accumulation in secretive cells through co-exposure to a clathrin-mediated endocytosis inhibitor (chlorpromazine), and proved the essential role of active endocytosis in the PS-NPs uptaking into entcrocyte cells. Our work not only elucidated the potential uptake and toxicity of PS-NPs in human intestinal cells and the underlying mechanism, but also provide a potential therapeutic approach to relieve the toxicity of PS-NPs to human through the endocytosis inhibition.

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