Kustra Agata, Zając Mirosław, Bednarczyk Piotr, Maliszewska-Olejniczak Kamila
Department of Physics and Biophysics, Institute of Biology, Warsaw University of Life Sciences- SGGW, Warsaw, Poland.
Biol Res. 2025 Jul 11;58(1):49. doi: 10.1186/s40659-025-00629-y.
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.
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.
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.
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.
最近的研究强调了环境暴露于纳米塑料对健康的严重影响,特别是其对人类胃肠道细胞的影响。在本研究中,我们使用人结肠腺癌(Caco-2)细胞来研究聚苯乙烯纳米颗粒(PNP)对细胞过程和DNA修复的影响。
我们将Caco-2细胞暴露于不同浓度的PNP,并监测细胞毒性、活性氧水平、聚(ADP-核糖)聚合酶-1(PARP-1)依赖性凋亡、DNA损伤以及DNA损伤反应(DDR)基因表达的变化。
结果表明,尽管彗星试验和γH2AX染色证明PNP不会直接导致单链断裂(SSB)或双链断裂(DSB),但它们会诱导氧化应激并显著改变DDR所需基因的表达。特别是,参与碱基切除修复(BER)途径和DSB修复的关键基因被下调,这表明细胞修复氧化DNA损伤的能力可能受损。
本研究强调了纳米塑料对肠道屏障细胞的亚致死效应。它强调了暴露于这些环境污染物可能带来的风险,这可能导致基因组不稳定和其他长期健康后果。