甲醛复合PM2.5致小鼠血液毒性的研究

摘要

In order to explore the influence and the underlying mechanism of FA and PM2.5on hepatotoxicity,we conducted systematic research from three aspects,including toxicity of blood,hematopoietic organs (bone marrow,spleen) and myeloid progenitor.Male Blab/c mice were taken as experimental object,and were randomly divided into four groups:the control group;PM2.5-exposure group;FA-exposure group;PM2.5 + FA-exposure group.Blood samples were firstly collected from mice caudal vein to conduct the complete blood count.Then the histopathological change of bone marrow and spleen (H & E staining) were observed.Furthermore,the oxidative damage (ROS,GSH),DNA damage (DPC,8-OH-dG) and apoptosis (caspase-3) in bone marrow,spleen and myeloid progenitor were detected.Results showed different degree of pathological changes in the bone marrow,spleen;compared with control group,oxidative damage,DNA damage,cell apoptosis level all demonstrated a rising trend in PM2.5,FA,PM2.5 + FA group.In conclusion,an exposure combined formaldehyde and PM2.5 could cause hepatotoxicity in mice,with a possible mechanism from oxidative stress as well as its downstream DNA damage.%为探究甲醛(FA)复合PM2.5对小鼠血液毒性的影响及其可能的机制,分别从血液,造血器官(骨髓、脾脏),髓系祖细胞3个层面的损伤进行系统研究.以雄性Balb/c小鼠为实验对象,把小鼠随机分为4组(对照组、PM2.5组、FA组、PM2.5+ FA组),对小鼠进行全血细胞计数;观察骨髓、脾脏病理学的变化;检测骨髓、脾脏及髓系祖细胞的氧化损伤(ROS,GSH),DNA损伤(DPC,8-OH-dG),细胞凋亡(caspase-3)指标.结果表明,骨髓、脾脏分别出现不同程度的病理学变化;骨髓、脾脏,髓系祖细胞的氧化损伤,DNA损伤,细胞凋亡水平也有上升趋势.FA复合PM2.5暴露会导致小鼠的血液毒性,氧化应激,及其下游的DNA损伤可能是FA复合PM2.5致小鼠血液毒性的一种重要机制.