Study On Acute Injury And Biomarker Of Respiratory System In Rats Induced By Airborne PM_2.5

The pollution of atmospheric particulate matters is closely associated with healtheffects. At present, the pollution and health hazard of particulate matters has receivedwidespread attention. A large number of epidemiological and toxicological datasuggests that the rise of particulate matters, especially the fine particulate matter (PM2.5)levels, may cause respiratory system, cardiovascular system and immune system disease.Although the study of PM2.5is increasing, the mechanism of respiratory damage causedby PM2.5is not fully clarified so far.In the study, twenty four male Wistar rats were randomly divided into four groups,including one saline control group and three PM2.5treatment groups. The experimentalPM2.5suspension was prepared in normal saline and endotracheally instilled to Wistarrats at levels of0,2.5,5,10mg/kg body weight (n=6per group). Exposures were for3consecutive days, every treatment interval of24h.The rats were sacrificed24hours afterthe latest treatment. Parameters of reactive oxygen species(ROS), mitochondrialmembrane potential(MMP), Ca2＋in pneumonocyte, enzymes(lactate dehydrogenaseLDH, acidic phosphatase ACP, alkaline phosphatase AKP), immune globulins IgG, IgA,IgM in bronchoalveolar lavage fluid(BALF) and cytokines related to bothpro-inflammation (tumor necrosis factor-alpha TNF-ɑ, interleukin-8IL-8)andanti-inflammation(interleukin-4IL-4, interleukin-10IL-10) were assayed. Meantime,pulmonary pathology and cell classification of the precipitated cell in BALF were alsoanalyzed.Results: Histopathological estimate of lung sections demonstrated that PM2.5inducedinfiltration of inflammatory cell, pulmonary interstitial hyperplasia and increasededema fluid in some animals. Besides, with the increase of instilled dose, the lesionseverity has a tendency to worsen. The percentage of the main immune cells in BALF(bronchoalveolar lavage fluid) was varied, a significant increment was observed inneutrophil percentage. There were no significant difference in enzyme, cytokine and immunoglobulin between the control and the exposure groups. Only the amounts ofAKP in the5.0mg/kg and10.0mg/kg level PM2.5group decreased significantlycompared with the control group. The level of Ca2＋increased significantly while theMMP decreased significantly in lung cells compared with the control group (P<0.05).The content of ROS in each dose group showed a trend of increase when compared withthe control group, but only the5.0mg/kg level PM2.5group reached statisticalsignificance. The experimental results suggested that airborne PM2.5could lead to acutelung injury, inflammation and oxidative stress may play an important role in the injury.The intracellular Ca2＋concentration and mitochondrial membrane potential can beused as sensitive biomarkers reflecting the acute PM2.5injury.