Alveolar Type II Cell Damage and Nrf2-SOD1 Pathway Downregulation Are Involved in PM(2.5)-Induced Lung Injury in Rats

The general toxicity of fine particulate matter (PM(2.5)) has been intensively studied, but its pulmonary toxicities are still not fully understood. To investigate the changes of lung tissue after PM(2.5) exposure and identify the potential mechanisms of pulmonary toxicity, PM(2.5) samples were firstly collected and analyzed. Next, different doses of PM(2.5) 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 PM(2.5) mass were organic carbon, elemental carbon, sulfate, nitrate, and ammonium. Different concentrations of PM(2.5) 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 PM(2.5) exposure, which was related to PM(2.5)-induced oxidative stress. These results provide a basis for a better understanding of pulmonary impairment in response to PM(2.5).