The Toxicological Mechanism Of Wintertime Haze PM_2.5 On Damages Of Alveolar Macrophages In Vitro

With the acceleration of urbanization, haze day have occurred at the times over the country, recently. So health effects and toxicological mechanism of haze has been paid more attention by scholars and the government. Atmospheric fine particulate matter (PM2.5, Particulate Matter≤2.5μm) is the primary pollutant, it is easier to absorb toxic and hazardous substances (such as heavy metals, volatile organic compounds and polycyclic aromatic hydrocarbons) for its small particle size and large specific surface area, PM2.5 can reach the alveoli and even spread to various organs of the body through the blood circulation system. Thus it do serious harm to human health.To investigate the toxicities of urban haze PM2.5 in Taiyuan to alveolar macrophages (AMs), AMs of rats were exposed to the ambient PM2.5 collected during a heavy haze episode with the doses of 0、33、100 and 300 μg·mL-1. The cell viability was detected using the MTT assay. The levels of cellular superoxide dismutase(SOD)、Glutathione peroxidase(GSH-Px)、Malondialdehyde(MDA)、Acid Phosphatase(ACP)、 Lactate Dehydrogenase(LDH) and Ca2+ in AMs were determined by a multimode reader. And reactive oxygen spcies (ROS) and cell apoptosis were observed by flow cytometry (FCM). The mRNA and protein level of apoptosis-related genes (Bax, Bcl-2 and p53) were measured by RT-PCR and Western blot, respectively. All these aimed to detect the toxicology of haze PM2.5 to AM from oxidative damage and apoptosis.The results showed:(1) PM2.5 increased MDA content, ACP activities and decreased the activities of SOD、 GSH-Px and LDH. Theses observations suggested that PM2.5 can cause oxidative damages to AMs. (2) AMs were exposed to PM2.5 in different doses, the level of ROS and Ca2+ increased significantly, the mRNA and protein expression levels of apoptosis-related genes p53 were upregulated, and the value of Bax/bcl-2 increased too. These results suggested that AM apoptosis probably caused by excessive ROS and Ca2+ accumulation.In conclusion, haze PM2.5 can cause oxidative damages to AMs and then induce the AM apoptosis, which likely being one of its toxicological way.