Study Of Haze PM_2.5 Toxicity On Alveolar Macrophages

With the continuous increase of environmental pollution, haze weather occurred frequently, and the harm of particulate pollution on the environment and human increased obviously. PM2.5(Particulate Matter<2.5, PM2.5),which has small particle size and large specific surface area is the primary pollutant of haze weather. It is easy to carry toxic and harmful substances. Therefore, long-term effect of exposure to low-level of PM2.5-induced health problems is particularly important. Recent studies have found that the occurrence of lung disease associated with PM2.5 which is not only lead to oxidative damage of alveolar macrophages (Alveolar Macrophage, AM), but also cause the change of structure, function and the size of mitochondrial. So, we study the damage of PM2.5 on AM.Firstly, the concentration of PM2.5 in haze day is 0.665 ± 0.275 mg · m-3, which is 12 times of the normal weather. The content of heavy metals Zn, Pb, Hg and water-soluble ions SO42-’NO3- increase because of coal and vehicle exhausts.Secondly, AM which extract from Wistar rats were treated with PM2.5 at different concentrations (0、33、100、300 μg·mL-1) and the levels of lipid peroxidation, activity of SOD、GSH-Px、ACP and LDH were determined to verify the toxicity induced by PM2.5.The results show that PM2.5 cause the increase of MDA content, ACP activities and the decrease of GSH-Px、SOD and LDH activity. These results suggest that PM2.5 cause oxidative damage to AM.Thirdly, the expression level of Mitochondrial fusion/fission genes including Mfn1、Mfn2、OPA1、Fis1、Drp1 by RT-PCR are measured. The results show that mitochondrial fusion genes expression augmented after PM2.5 exposure.Finally, AM mitochondria number decreasing, volume increase and megamitochondrion is observed with laser scanning confocal microscopy. Meanwhile, Ultrastructural results of AM verify it.In conclusion, the water-soluble ions and insoluble components in haze PM2.5 cause the damage on AM. It can cause oxidative damage, change the mitochondrial fusion and fission on AM and induce megamitochondrion. The results will provide theory evidence for the toxic effects of PM2.5 exposure.