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Background <p>Recent studies have highlighted the critical health implications of environmental exposure to nanoplastics, particularly concerning their effects on human gastrointestinal cells. In this study, we used human colorectal adenocarcinoma (Caco-2) cells to investigate the exposure of polystyrene nanoparticles (PNPs) to cellular processes and DNA repair.</p> Methods <p>We exposed Caco-2 cells to various concentrations of PNPs and monitored cytotoxicity, ROS levels, PARP-1-dependent apoptosis, DNA damage, and changes in DNA damage response (DDR) gene expression.</p> Results <p>The results indicated that although PNPs did not directly cause SSBs or DSBs, as evidenced by comet assays and γH2AX staining, they induced oxidative stress and significantly altered the expression of genes required for DDR. In particular, critical genes involved in the base excision repair (BER) pathway and DSBs repair were downregulated, suggesting a potential impairment of the cell’s ability to repair oxidative DNA damage.</p> Conclusions <p>This study highlights the sublethal effects of nanoplastics on intestinal barrier cells. It underscores the possible risks of exposure to these environmental contaminants, which can lead to genome instability and other long-term health consequences.</p>

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Exposure to polystyrene nanoparticles leads to dysfunction in DNA repair mechanisms in Caco-2 cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月11日

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  • Agata Kustra,
  • Mirosław Zając,
  • Piotr Bednarczyk,
  • Kamila Maliszewska-Olejniczak

摘要

Background

Recent studies have highlighted the critical health implications of environmental exposure to nanoplastics, particularly concerning their effects on human gastrointestinal cells. In this study, we used human colorectal adenocarcinoma (Caco-2) cells to investigate the exposure of polystyrene nanoparticles (PNPs) to cellular processes and DNA repair.

Methods

We exposed Caco-2 cells to various concentrations of PNPs and monitored cytotoxicity, ROS levels, PARP-1-dependent apoptosis, DNA damage, and changes in DNA damage response (DDR) gene expression.

Results

The results indicated that although PNPs did not directly cause SSBs or DSBs, as evidenced by comet assays and γH2AX staining, they induced oxidative stress and significantly altered the expression of genes required for DDR. In particular, critical genes involved in the base excision repair (BER) pathway and DSBs repair were downregulated, suggesting a potential impairment of the cell’s ability to repair oxidative DNA damage.

Conclusions

This study highlights the sublethal effects of nanoplastics on intestinal barrier cells. It underscores the possible risks of exposure to these environmental contaminants, which can lead to genome instability and other long-term health consequences.