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基金项目：国家自然科学基金(No.21177078);山西省自然科学基金(No.2011011009-2);山西省回国留学人员科研资助项目(No.2013-012)

摘要：为研究太原市冬季灰霾天气下大气PM_2.5对肺泡巨噬细胞(AM)的毒性作用,采用采集于2011年12月30—31日的灰霾PM_2.5悬浮液体外处理大鼠AM(终浓度分别为0、33、100、300 μg·mL^-1),用MTT法检测细胞活力,用酶标仪测定胞内超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)及Ca²⁺浓度,并用流式细胞仪测定胞内活性氧(ROS)和细胞凋亡状况.结果表明:随着PM_2.5浓度增大,AM存活率、SOD和GSH-Px活性下降,MDA及ROS含量和Ca²⁺浓度升高,均呈现剂量-效应关系,细胞早期凋亡率也随着染毒浓度的增加呈现升高趋势,揭示了太原市灰霾PM_2.5可使AM产生氧化应激,引起细胞脂质过氧化损伤和凋亡发生.

Abstract：To investigate the toxicities of PM_2.5 (particulate matter less than 2.5 μm in aerodynamic diameter) on alveolar macrophages (AMs), the rat AMs were exposed to the ambient PM_2.5 with final dosages of 0, 33, 100 and 300 μg·mL^-1 collected during a heavy haze episode. The cell viability was detected using the MTT assay. The levels of cellular superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and Ca²⁺ in AMs were determined by a multimode reader. And the reactive oxygen species (ROS) and apoptotic cells were observed by using a flow cytometry (FCM). Results showed that PM_2.5 resulted in an increase of ROS, Ca²⁺, and MDA content in AMs and a decrease of cell viability and SOD and GSH-Px activities in a dose-dependent manner. Furthermore, the cell apoptosis rate increased with the increasing of PM_2.5 treatment concentration. These observations suggested that haze PM_2.5 can cause oxidative damages on AMs and then induce the AM apoptosis, likely being one of its toxicological mechanisms.