Background & Aim: Fine particulate matter (PM 2.5) is deemed a carcinogenic factor and one of the most dangerous health causes with persistent high ambient concentrations. Researchers are continuing to explore the toxicity mechanism and also solutions to regulate the effect of harmful components of PM2.5.
Our goal was to reveal mitochondria as a therapy to prevent and destroy fine particle exposure. In this study, we used human lung cancer cells (A594) exposed to PM2.5 as a positive control and evaluated the effects on proliferation, apoptosis, cellular aging, and reactive oxygen species (ROS) production.

Methods, Results & Conclusion: PM2.5 was prepared for treatment; invasion and migration tests were performed, and its toxicity and effect on A549 cells were examined using a microfluidic device to demonstrate ROS production, which has been verified through ROS detection assay and JC1 assay was investigated under continuous PM2.5 treatment with or without receive allogenic mitochondria. Others, mitochondria were isolated from healthy donors and transported into PM2.5-administrated A594 cells.
Results of RNA sequencing revealed 423 genes that displayed significant differential expression in response to PM2.5 exposure, with a particular focus on pathways associated with the generation of reactive oxygen species (ROS) and mitochondrial dysfunction. Real-time detection demonstrated an increase in ROS production in A549 cells after exposure to PM2.5. JC1 assay, which indicated a loss of mitochondrial membrane potential (ΔΨm) in A549 cells exposed to PM2.5. The disruption of mitochondrial membrane potential further supports the detrimental effects of PM2.5 on A549 cells. Additionally, apoptosis analysis showed a higher percentage of early apoptosis in PM2.5-exposed cells compared to the control group.
These findings highlight several adverse effects of PM2.5 on A549 cells, including enhanced invasion and migration capabilities, altered gene expression related to ROS pathways, increased ROS production, induction of apoptosis, and disruption of mitochondrial membrane potential. Through the transfer of healthy mitochondria from donors into PM2.5-exposure A594 cells, these findings contribute to our understanding of the potential mechanisms through which PM2.5 can impact cellular function and health.

Uyen Nguyen Thi Nhat

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