Related Experiment Video
Updated: Apr 19, 2026
Analysis of the Ambient Particulate Matter-induced Chromosomal Aberrations Using an In Vitro System
Published on: December 21, 2016
Effect of ambient PM(2.5) on lung mitochondrial damage and fusion/fission gene expression in rats
Ruijin Li1, Xiaojing Kou, Hong Geng
1Institute of Environmental Science, College of Environmental & Resource Sciences, Shanxi University , Taiyuan 030006, China.
Abstract:
Exposure to ambient fine particulate matter (PM2.5) increases the risk of respiratory disease. Although previous mitochondrial research has provided new information about PM toxicity in the lung, the exact mechanism of PM2.5-mediated structural and functional damage of lung mitochondria remains unclear. In this study, changes in lung mitochondrial morphology, expression of mitochondrial fission/fusion markers, lipid peroxidation, and transport ATPase activity in SD rats exposed to ambient PM2.5 at different dosages were investigated. Also, the release of reactive oxygen species (ROS) via the respiratory burst in rat alveolar macrophages (AMs) exposed to PM2.5 was examined by luminol-dependent chemiluminescence (CL). The results showed that (1) PM2.5 deposited in the lung and induced pathological damage, particularly causing abnormal alterations of mitochondrial structure, including mitochondrial swelling and cristae disorder or even fragmentation in the presence of higher doses of PM2.5; (2) PM2.5 significantly affected the expression of specific mitochondrial fission/fusion markers (OPA1, Mfn1, Mfn2, Fis1, and Drp1) in rat lung; (3) PM2.5 inhibited Mn superoxide dismutase (MnSOD), Na(+)K(+)-ATPase, and Ca(2+)-ATPase activities and elevated malondialdehyde (MDA) content in rat lung mitochondria; and (4) PM2.5 induced rat AMs to produce ROS, which was inhibited by about 84.1% by diphenyleneiodonium chloride (DPI), an important ROS generation inhibitor. It is suggested that the pathological injury observed in rat lung exposed to PM2.5 is associated with mitochondrial fusion-fission dysfunction, ROS generation, mitochondrial lipid peroxidation, and cellular homeostasis imbalance. Damage to lung mitochondria may be one of the important mechanisms by which PM2.5 induces lung injury, contributing to respiratory diseases.
Insights
Fine particulate matter (PM2.5) damages lung mitochondria, causing structural changes and dysfunction. This mitochondrial injury, including ROS generation and lipid peroxidation, contributes to PM2.5-induced respiratory diseases.
Area of Science:
- Environmental Health
- Toxicology
- Mitochondrial Biology
Background:
- Ambient fine particulate matter (PM2.5) is a known risk factor for respiratory diseases.
- The precise mechanisms of PM2.5-induced lung mitochondrial damage are not fully understood.
- Mitochondrial dysfunction plays a role in PM toxicity within the lungs.
Purpose of the Study:
- To investigate the effects of PM2.5 exposure on lung mitochondrial structure and function in Sprague-Dawley (SD) rats.
- To examine the impact of PM2.5 on mitochondrial morphology, fission/fusion markers, lipid peroxidation, and ATPase activity.
- To assess PM2.5-induced reactive oxygen species (ROS) generation in rat alveolar macrophages (AMs).
Main Methods:
- Rats were exposed to varying dosages of ambient PM2.5.
- Lung mitochondrial morphology and expression of fission/fusion markers (OPA1, Mfn1, Mfn2, Fis1, Drp1) were analyzed.
- Mitochondrial enzyme activities (MnSOD, Na(+)K(+)-ATPase, Ca(2+)-ATPase) and malondialdehyde (MDA) content were measured.
- ROS production in AMs was assessed using luminol-dependent chemiluminescence (CL).
Main Results:
- PM2.5 exposure led to pathological lung damage and abnormal mitochondrial structure, including swelling and fragmentation at higher doses.
- Significant alterations in mitochondrial fission/fusion marker expression were observed in rat lungs.
- PM2.5 inhibited MnSOD, Na(+)K(+)-ATPase, and Ca(2+)-ATPase activities while increasing MDA levels in lung mitochondria.
- PM2.5 exposure stimulated ROS production in rat AMs, with significant inhibition by diphenyleneiodonium chloride (DPI).
Conclusions:
- PM2.5-induced lung injury is linked to mitochondrial fusion-fission imbalance, ROS generation, lipid peroxidation, and cellular homeostasis disruption.
- Damage to lung mitochondria is a key mechanism underlying PM2.5-mediated respiratory disease.
- Understanding these mechanisms can inform strategies for mitigating PM2.5 health effects.
More Related Videos
12:15Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
Published on: May 29, 2019
05:58Using Immunofluorescence to Detect PM2.5-induced DNA Damage in Zebrafish Embryo Hearts
Published on: February 15, 2021