Alveolar Type II Cell Damage and Nrf2-SOD1 Pathway Downregulation Are Involved in PM2.5-Induced Lung Injury in Rats

Abstract

The general toxicity of fine particulate matter (PM2.5) has been intensively studied, but its pulmonary toxicities are still not fully understood. To investigate the changes of lung tissue after PM2.5 exposure and identify the potential mechanisms of pulmonary toxicity, PM2.5 samples were firstly collected and analyzed. Next, different doses of PM2.5 samples (5 mg/kg, 10 mg/kg, 20 mg/kg) were intratracheally instilled into rats to simulate lung inhalation of polluted air. After instillation for eight weeks, morphological alterations of the lung were examined, and the levels of oxidative stress were detected. The data indicated that the major contributors to PM2.5 mass were organic carbon, elemental carbon, sulfate, nitrate, and ammonium. Different concentrations of PM2.5 could trigger oxidative stress through increasing reactive oxygen species (ROS) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, and decreasing expression of antioxidant-related proteins (nuclear factor erythroid 2-related factor 2 (Nrf2), superoxide dismutase 1 (SOD1) and catalase). Histochemical staining and transmission electron microscopy displayed pulmonary inflammation, collagen deposition, mitochondrial swelling, and a decreasing number of multilamellar bodies in alveolar type II cells after PM2.5 exposure, which was related to PM2.5-induced oxidative stress. These results provide a basis for a better understanding of pulmonary impairment in response to PM2.5.

The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease

“… 94 After being exposed to PM2.5, it is observed that there are fewer multilamellar bodies in the Alveolar epithelial type II; cell (AT2) increases mitochondrial swelling, collagen deposition, and pulmonary inflammation. 95 In addition, it can be observed that the dysregulated AT2 cells into AT1 cells in the PM2.5-induced COPD mouse model 96 damage cellular repair mechanisms. Even worse, it has been shown that inflamed bronchial epithelial cells caused by air pollution particles trigger apoptosis, 97 particularly when PM2.5 is injected into those inflamed by cigarettes.…”