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PM2.5/O3暴露损伤细胞及线粒体的分子调控机制差异

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吴婷婷, 魏永杰, 李志刚. PM2.5/O3暴露损伤细胞及线粒体的分子调控机制差异[J]. 生态毒理学报, 2025, 20(1): 77-94. doi: 10.7524/AJE.1673-5897.20240716001
引用本文: 吴婷婷, 魏永杰, 李志刚. PM2.5/O3暴露损伤细胞及线粒体的分子调控机制差异[J]. 生态毒理学报, 2025, 20(1): 77-94. doi: 10.7524/AJE.1673-5897.20240716001
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WU Tingting, WEI Yongjie, LI Zhigang. Differences in Molecular Regulatory Mechanisms of Cells and Mitochondria Damaged by PM2.5/O3 Exposure[J]. Asian journal of ecotoxicology, 2025, 20(1): 77-94. doi: 10.7524/AJE.1673-5897.20240716001
Citation: WU Tingting, WEI Yongjie, LI Zhigang. Differences in Molecular Regulatory Mechanisms of Cells and Mitochondria Damaged by PM2.5/O3 Exposure[J]. Asian journal of ecotoxicology, 2025, 20(1): 77-94. doi: 10.7524/AJE.1673-5897.20240716001
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PM2.5/O3暴露损伤细胞及线粒体的分子调控机制差异

  • 1. 中国环境科学研究院 环境基准与风险评估国家重点实验室, 北京 100012;

  • 2. 同济大学环境科学与工程学院, 上海 200092

    • 作者简介: 吴婷婷(1999—)，女，博士，研究方向为环境毒理学和分子毒理学，E-mail:2524369560@qq.com;wutingting777@yeah.net
    通讯作者: 李志刚,E-mail:lizg@craes.org.cn
  • 基金项目:

    科技部重点研发计划项目(2022YFC3702603，2022YFC3703000)

  • 中图分类号: X171.5

Differences in Molecular Regulatory Mechanisms of Cells and Mitochondria Damaged by PM2.5/O3 Exposure

  • 1. State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing 100012, China;

  • 2. College of Environmental Science and Engineering, Tongji University, Shanghai 200092, China

    • Corresponding author: LI Zhigang, lizg@craes.org.cn
  • Fund Project:

  • 摘要: 流行性病学研究表明，PM2.5和O3均与一些不良健康结局相关，如心肺、神经系统等相关疾病。在健康结局层面，PM2.5和O3的暴露效果具有一定的相似性。然而，PM2.5/O3的理化性质具有显著差异：PM2.5是分散在大气中呈固态或液态的颗粒物；而O3是具有强氧化性质的气体。生物体对不同性质的干扰有不同的防御及反应机制，故推测二者导致疾病发生的过程及分子调控机制可能存在差异。体外实验综述表明，氧化应激是PM2.5及O3造成损伤的重要机制。在细胞层面，PM2.5主要通过诱导细胞内自噬相关的炎症反应发挥作用；而O3通过攻击细胞膜上不饱和结构导致膜损伤。线粒体产能过程伴随着活性氧(ROS)的产生。当外界环境变化，细胞内的ROS平衡被打破，进而导致线粒体损伤。线粒体在细胞发育、代谢、信号传导及细胞命运调控等方面起着关键作用。近年来在线粒体层面的研究表明，PM2.5暴露可引起细胞内离子变化，诱导与线粒体相关的生理变化；而O3作为氧化分子直接损伤线粒体。本文综述了PM2.5/O3暴露导致的线粒体结构、功能、线粒体DNA (mtDNA)及相关信号通路的损伤机制，进一步探讨了二者在健康结局和疾病发生中的异同。通过阐明PM2.5/O3对线粒体及细胞损伤的机制，本文为大气污染相关疾病的预防和诊断提供了新的思路和研究方向。
    Abstract: Epidemiological studies have shown that PM2.5 and O3 are associated with some adverse health outcomes, such as cardiopulmonary, neurological, and other system-related diseases. These adverse health outcomes induced by PM2.5 and O3 are similar. PM2.5 and O3 have distinct physical and chemical properties, with PM2.5 being a solid-liquid mixture and O3 being a strongly oxidizing gaseous pollutant. Biological organisms have distinct defense and response mechanisms for different environmental disturbances. Therefore, it is hypothesized that the processes and molecular regulatory mechanisms of diseases induced by PM2.5 and O3 exposure could be different. In vitro studies suggested that oxidative stress is an essential mechanism of damage caused by PM2.5/O3. At the cellular level, PM2.5 primarily exerts its effects by inducing autophagy-related inflammatory responses, whereas O3 leads to membrane damage by attacking unsaturated structures in the cell membrane. The process of mitochondrial energy production is accompanied by the generation of reactive oxygen species (ROS). The imbalance of ROS oxidative and antioxidant reactions induced by PM2.5 and O3 exposure could lead to mitochondrial damage. Mitochondria play an essential role in cell development, metabolism, signal transduction, and regulation of cell fate. Recent studies indicated that PM2.5 exposure induced mitochondrial-related physiological alterations by modulating intracellular ion dynamics. In contrast, O3, as a potent oxidizing agent, directly inflicted damage on cellular structures, including mitochondria. This review provides a comprehensive summary of the damage to mitochondrial structure, function, mitochondrial DNA (mtDNA), and related signaling pathways caused by PM2.5 and O3 exposure. Furthermore, it explores the similarities and differences in health outcomes and disease processes between PM2.5 and O3. By elucidating the damage mechanism of PM2.5 and O3 to mitochondria and cells, this article offers new insights and research directions for the prevention and diagnosis of diseases related to atmospheric pollution.
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  • 收稿日期:  2024-07-16
吴婷婷, 魏永杰, 李志刚. PM2.5/O3暴露损伤细胞及线粒体的分子调控机制差异[J]. 生态毒理学报, 2025, 20(1): 77-94. doi: 10.7524/AJE.1673-5897.20240716001
引用本文: 吴婷婷, 魏永杰, 李志刚. PM2.5/O3暴露损伤细胞及线粒体的分子调控机制差异[J]. 生态毒理学报, 2025, 20(1): 77-94. doi: 10.7524/AJE.1673-5897.20240716001
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WU Tingting, WEI Yongjie, LI Zhigang. Differences in Molecular Regulatory Mechanisms of Cells and Mitochondria Damaged by PM2.5/O3 Exposure[J]. Asian journal of ecotoxicology, 2025, 20(1): 77-94. doi: 10.7524/AJE.1673-5897.20240716001
Citation: WU Tingting, WEI Yongjie, LI Zhigang. Differences in Molecular Regulatory Mechanisms of Cells and Mitochondria Damaged by PM2.5/O3 Exposure[J]. Asian journal of ecotoxicology, 2025, 20(1): 77-94. doi: 10.7524/AJE.1673-5897.20240716001
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PM2.5/O3暴露损伤细胞及线粒体的分子调控机制差异

    通讯作者: 李志刚,E-mail:lizg@craes.org.cn
    作者简介: 吴婷婷(1999—)，女，博士，研究方向为环境毒理学和分子毒理学，E-mail:2524369560@qq.com;wutingting777@yeah.net
  • 1. 中国环境科学研究院 环境基准与风险评估国家重点实验室, 北京 100012;
  • 2. 同济大学环境科学与工程学院, 上海 200092
  • 收稿日期:  2024-07-16
基金项目:

科技部重点研发计划项目(2022YFC3702603，2022YFC3703000)

摘要: 流行性病学研究表明，PM2.5和O3均与一些不良健康结局相关，如心肺、神经系统等相关疾病。在健康结局层面，PM2.5和O3的暴露效果具有一定的相似性。然而，PM2.5/O3的理化性质具有显著差异：PM2.5是分散在大气中呈固态或液态的颗粒物；而O3是具有强氧化性质的气体。生物体对不同性质的干扰有不同的防御及反应机制，故推测二者导致疾病发生的过程及分子调控机制可能存在差异。体外实验综述表明，氧化应激是PM2.5及O3造成损伤的重要机制。在细胞层面，PM2.5主要通过诱导细胞内自噬相关的炎症反应发挥作用；而O3通过攻击细胞膜上不饱和结构导致膜损伤。线粒体产能过程伴随着活性氧(ROS)的产生。当外界环境变化，细胞内的ROS平衡被打破，进而导致线粒体损伤。线粒体在细胞发育、代谢、信号传导及细胞命运调控等方面起着关键作用。近年来在线粒体层面的研究表明，PM2.5暴露可引起细胞内离子变化，诱导与线粒体相关的生理变化；而O3作为氧化分子直接损伤线粒体。本文综述了PM2.5/O3暴露导致的线粒体结构、功能、线粒体DNA (mtDNA)及相关信号通路的损伤机制，进一步探讨了二者在健康结局和疾病发生中的异同。通过阐明PM2.5/O3对线粒体及细胞损伤的机制，本文为大气污染相关疾病的预防和诊断提供了新的思路和研究方向。

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