甲醛复合PM2.5致小鼠血液毒性的研究

Formaldehyde and PM_(2.5) induced hepatotoxicity in mice

为探究甲醛(FA)复合PM_(2.5)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、PM_(2.5)组、FA组、PM_(2.5)+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-d G),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PM_(2.5)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PM_(2.5)致小鼠血液毒性的一种重要机制.

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 PM2.5could cause hepatotoxicity in mice,with a possible mechanism from oxidative stress as well as its downstream DNA damage.