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<p>Silver Selenide quantum dots (Ag<sub>2</sub>Se QDs) have great potential for biomedical applications due to their excellent optical properties, which has raised concerns about their health hazards. Previous studies have shown that exposure to Ag<sub>2</sub>Se QDs can induce neurotoxicity, but the underlying mechanisms have not been fully elucidated. In this study, Ag<sub>2</sub>Se QDs activated Nod-like receptor protein 3 (NLRP3) inflammasomes in microglia. Interestingly, we found that Ag<sub>2</sub>Se QDs-induced NLRP3 inflammasome activation was ferroptosis-dependent. Mechanistically, the overproduction of mitochondrial reactive oxygen species (mtROS) led to the leakage of mitochondrial DNA (mtDNA) into the cytoplasm <i>via</i> the open mitochondrial permeability transition pore (mPTP), thereby activating stimulator of interferon genes (STING)-dependent ferritinophagy. Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy resulted in the degradation of ferritin heavy chain 1 (FTH1) and the release of iron ions, ultimately triggering ferroptosis. In order to assist in the risk assessment of Ag<sub>2</sub>Se QDs and the development of risk management strategies. Based on the above experimental data, we constructed an Adverse Outcome Pathway (AOP) framework for Ag<sub>2</sub>Se QDs neurotoxicity and emphasized the significance of alleviating mitochondrial damage in preventing neurotoxicity. Overall, the present study reveals new mechanisms of Ag<sub>2</sub>Se QDs-induced neurotoxicity. Meanwhile, this study provides insightful references for toxicity assessment and address.</p> Graphical Abstract <p></p>

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Ag2Se quantum dots neurotoxicity: mitochondrial stress drives ferroptosis-dependent microglial inflammation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月2日

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  • Yongshuai Yao,
  • Zhihui Wang,
  • Chunhui Zhang,
  • Xiaoquan Huang,
  • Tingting Wei,
  • Na Liu,
  • Lingyue Zou,
  • Changcun Bai,
  • Yuanyuan Hu,
  • Qing Fang,
  • Min Chen,
  • Shujing Guan,
  • Yuying Xue,
  • Tianshu Wu,
  • Ting Zhang,
  • Meng Tang

摘要

Silver Selenide quantum dots (Ag2Se QDs) have great potential for biomedical applications due to their excellent optical properties, which has raised concerns about their health hazards. Previous studies have shown that exposure to Ag2Se QDs can induce neurotoxicity, but the underlying mechanisms have not been fully elucidated. In this study, Ag2Se QDs activated Nod-like receptor protein 3 (NLRP3) inflammasomes in microglia. Interestingly, we found that Ag2Se QDs-induced NLRP3 inflammasome activation was ferroptosis-dependent. Mechanistically, the overproduction of mitochondrial reactive oxygen species (mtROS) led to the leakage of mitochondrial DNA (mtDNA) into the cytoplasm via the open mitochondrial permeability transition pore (mPTP), thereby activating stimulator of interferon genes (STING)-dependent ferritinophagy. Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy resulted in the degradation of ferritin heavy chain 1 (FTH1) and the release of iron ions, ultimately triggering ferroptosis. In order to assist in the risk assessment of Ag2Se QDs and the development of risk management strategies. Based on the above experimental data, we constructed an Adverse Outcome Pathway (AOP) framework for Ag2Se QDs neurotoxicity and emphasized the significance of alleviating mitochondrial damage in preventing neurotoxicity. Overall, the present study reveals new mechanisms of Ag2Se QDs-induced neurotoxicity. Meanwhile, this study provides insightful references for toxicity assessment and address.

Graphical Abstract