Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in rat alveolar macrophages

Although positive associations exist between ambient particulate matter (PM2.5; diameter <= 2.5 mu m) and the morbidity and mortality rates for respiratory diseases, the biological mechanisms of the reported health effects are unclear. Considering that alveolar macrophages (AM) are the main cells responsible for phagocytic clearance of xenobiotic particles that reach the airspaces of the lungs, the purpose of this study was to investigate whether PM2.5 induced AM apoptosis, and investigate its possible mechanisms. Freshly isolated AM from Wistar rats were treated with extracted PM2.5 at concentrations of 33, 100, or 300 mu g/mL for 4 h; thereafter, the cytotoxic effects were evaluated. The results demonstrated that PM2.5 induced cytotoxicity by decreasing cell viability and increasing lactate dehydrogenase (LDH) levels in AMs. The levels of reactive oxygen species (ROS) and intracellular calcium cations (Ca2+) markedly increased in higher PM2.5 concentration groups. Additionally, the apoptotic ratio increased, and the apoptosis-related proteins BCL2-associated X (Bax), caspase-3, and caspase-9 were upregulated, whereas B cell lymphoma-2 (Bcl-2) protein levels were downregulated following PM2.5 exposure. Cumulative findings showed that PM2.5 induced apoptosis in AMs through a mitochondrial-mediated pathway, which indicated that PM2.5 plays a significant role in lung injury diseases.

Automated summary

PM2.5 can induce apoptosis in alveolar macrophages, causing cytotoxic effects, increasing levels of reactive oxygen species and intracellular calcium ions, and leading to lung injury diseases through a mitochondrial-mediated pathway.