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<p>Silver nanoparticles (AgNPs) are engineered nanomaterials composed of silver atomic clusters with sizes ranging from 1 to 100&#xa0;nm. These particles have gained widespread application in food and medicine due to their potent broad-spectrum antibacterial properties. As research on AgNPs has advanced, increasing attention has focused on their cytotoxic mechanisms, particularly the phenomenon of mitochondrial targeting and subsequent cellular damage. However, the precise molecular pathways underlying these effects remain incompletely elucidated. In the present study, HeLa cells were exposed to 15&#xa0;nm AgNPs for 24&#xa0;h. Cell viability assays revealed a concentration-dependent decrease in survival when AgNP concentrations reached 16&#xa0;µg/mL. Notably, reverse transcription polymerase chain reaction (RT-PCR) analysis demonstrated unchanged expression levels of the <i>POLG2</i> gene, which encodes the accessory subunit (Polg2) of mitochondrial DNA polymerase gamma (Pol-γ). This observation suggests preserved nuclear integrity under these experimental conditions. Concomitant with these findings, quantitative analysis of mitochondrial DNA (mtDNA) content showed a significant increase in mtDNA copy number, implying compensatory mitochondrial proliferation secondary to damage. Further mechanistic investigation through immunoprecipitation assays revealed direct physical interaction between AgNPs and the Polg2 protein. Collectively, these results support a model wherein AgNP-induced mitochondrial dysfunction but not nuclear damage in cytotoxic pathways. The observed AgNP-Polg2 interaction emerges as a critical factor in disrupting mitochondrial homeostasis, suggesting novel therapeutic targets for mitigating nanoparticle toxicity. We propose that after entering cells, AgNPs directly interact with mitochondrial DNA polymerase, thereby disrupting mitochondrial homeostasis and ultimately leading to cell death.</p>

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Silver nanoparticles induce binding of mitochondrial DNA polymerase gamma subunit Polg2 and mitochondrial dysfunction in HeLa cells

  • 期刊论文

  • 发表日期：

    2026年4月7日

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  • Xueling Peng,
  • Qingdai Liu

摘要

Silver nanoparticles (AgNPs) are engineered nanomaterials composed of silver atomic clusters with sizes ranging from 1 to 100 nm. These particles have gained widespread application in food and medicine due to their potent broad-spectrum antibacterial properties. As research on AgNPs has advanced, increasing attention has focused on their cytotoxic mechanisms, particularly the phenomenon of mitochondrial targeting and subsequent cellular damage. However, the precise molecular pathways underlying these effects remain incompletely elucidated. In the present study, HeLa cells were exposed to 15 nm AgNPs for 24 h. Cell viability assays revealed a concentration-dependent decrease in survival when AgNP concentrations reached 16 µg/mL. Notably, reverse transcription polymerase chain reaction (RT-PCR) analysis demonstrated unchanged expression levels of the POLG2 gene, which encodes the accessory subunit (Polg2) of mitochondrial DNA polymerase gamma (Pol-γ). This observation suggests preserved nuclear integrity under these experimental conditions. Concomitant with these findings, quantitative analysis of mitochondrial DNA (mtDNA) content showed a significant increase in mtDNA copy number, implying compensatory mitochondrial proliferation secondary to damage. Further mechanistic investigation through immunoprecipitation assays revealed direct physical interaction between AgNPs and the Polg2 protein. Collectively, these results support a model wherein AgNP-induced mitochondrial dysfunction but not nuclear damage in cytotoxic pathways. The observed AgNP-Polg2 interaction emerges as a critical factor in disrupting mitochondrial homeostasis, suggesting novel therapeutic targets for mitigating nanoparticle toxicity. We propose that after entering cells, AgNPs directly interact with mitochondrial DNA polymerase, thereby disrupting mitochondrial homeostasis and ultimately leading to cell death.