时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
It remains unclear whether chemically different nanoparticles converge on similar mitochondrial stress-response pathways while still showing particle-specific biological responses.Transition metal ions drive UFPM toxicity, redox cycling, and Fenton reactions, generating oxidative stress, ROS, and mitochondrial damage (3, 4).；These results also confirm the importance of oxidative and mitochondrial stress in the cellular response to PS-NPs exposure and the need to clarify whether similar stress responses are involved across different chemicals.；These results highlight a key research gap: whether chemically distinct nanoparticulate environmental contaminants use the same mitochondrial pathway or follow distinct stress-induced pathways that result in bioenergetic dysfunction and immunotoxicity.
方法
Thus, we established an exposure comparison model in which PBMCs were subjected to different environmentally relevant nanoparticles with unique chemical compositions under similar experimental conditions to study whether common or particle-specific mitochondrial stress adaptation pathways exist.；We hypothesized that although UFPMs, BC, and PS-NPs influence mitochondrial homeostasis, all three use a common mitochondrial stress response system, with particle-specific adaptations that lead to distinct molecular signatures and inflammation/immunotoxic effects.2Materials and methodsPBMCs were obtained from 30 healthy adult donors and exposed to UFPM, BC, and PS-NPs at a common mass concentration of 1 µg/mL for 6, 12, and 24 h (4, 8, 20, 30, 31) following the norms of the Institutional Ethics Committee [INTR-IM-2024-00063 (PKM)].；For molecular, biochemical, mitochondrial, and inflammatory endpoint analyses, cells were assessed after 6, 12, and 24 h of exposure, with an additional 48 h time point for flow-cytometric assessment of cellular oxidative stress and mitochondrial-associated fluorescence.
核心结论
These results also confirm the importance of oxidative and mitochondrial stress in the cellular response to PS-NPs exposure and the need to clarify whether similar stress responses are involved across different chemicals.；These results highlight a key research gap: whether chemically distinct nanoparticulate environmental contaminants use the same mitochondrial pathway or follow distinct stress-induced pathways that result in bioenergetic dysfunction and immunotoxicity.；Overall, DLS and zeta-potential analyses show that BC, PS-NPs, and UFPM exhibit distinct hydrodynamic and surface-charge properties.
局限
It remains unclear whether chemically different nanoparticles converge on similar mitochondrial stress-response pathways while still showing particle-specific biological responses.Transition metal ions drive UFPM toxicity, redox cycling, and Fenton reactions, generating oxidative stress, ROS, and mitochondrial damage (3, 4).；Nevertheless, the OMA1-DELE1-ISR pathway has recently been identified as a key orchestrator of mitochondrial stress adaptation; however, it remains unclear whether different nanoparticles use these pathways in distinct ways.；UFPMs, BC, and PS-NPs can activate mitochondrial stress through different upstream mechanisms that converge on the mitochondria, where common stress-response pathways are activated with NP-specific kinetics.However, if oxidative stress surpasses the mitochondria’s adaptive responses, it can damage many parts of the electron transport chain, impairing oxidative phosphorylation and energy production.
对本项目的价值
中高价值：属「线粒体质量控制与氧化应激」方向；线粒体功能与氧化应激栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.0/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 63,400 字符，题名指纹 0.94，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：保守与颗粒特异的线粒体应激反应驱动超细颗粒物、黑碳与聚苯乙烯纳米塑料的免疫毒性
- 英文标题：Conserved and particle-specific mitochondrial stress responses drive immunotoxicity of ultrafine particulate matter, black carbon, and polystyrene nanoplastics.
- 期刊与标识：Frontiers in immunology · PMID 42973590 · DOI 10.3389/fimmu.2026.1993305 · PMC PMC13724557