大气颗粒物对斑马鱼胚胎的毒性及机制研究进展

流行病学研究揭示PM_2.5暴露与低体重新生儿,早产,先兆子痫,自发性流产,胎儿心血管、消化和神经系统发育异常以及出生缺陷具有相关性,但PM_2.5对儿童发育影响的毒性机制尚不清楚。斑马鱼现已成为体内发育毒性研究的主要模式动物,综述了大气颗粒物对斑马鱼胚胎的毒性及机制相关研究进展,结果表明:大气颗粒物暴露可增加胚胎畸形率和死亡率,且效应强度与颗粒物来源和暴露方式有关;大气颗粒物还可造成胚胎骨骼、心脏、鱼鳔、肝、肠、肌肉等器官组织损伤;毒性机制主要包括改变胚胎全基因表达、microRNA表达及心脏AhR和Wnt/β-catenin通路相关基因表达,最终引起炎症和氧化应激过程,导致胚胎毒性和器官畸形,影响心血管、神经、运动等系统发育。

A review of toxicity and mechanism of atmospheric particulate matter on zebrafish embryos

Epidemiological studies have showed that low birth weight, preterm delivery, preeclampsia, spontaneous abortion, abnormal development of cardiovascular, digestive and nervous system, and birth defects in infants are associated with PM2.5 exposure. However, the toxic mechanism of PM2.5 on children’s development remains unclear. Zebrafish has been the main model animal of developmental toxicity research in vivo. The research progress of toxicity and mechanism of atmospheric particulate matter on zebrafish embryos was reviewed. It was revealed that atmospheric particulate matter exposure could cause an increase in embryo malformation rate and mortality, and the effect intensity was related to the source and exposure mode of particulate matter. Exposure to atmospheric particulate matter could damage the bones, heart, swim bladder, liver, bowel, muscle and other tissues. The toxicity mechanism mainly included changing the whole zebrafish embryo gene expression, microRNA expression, and heart AhR and Wnt/β-catenin pathway related gene expression, which eventually caused physiological process such as inflammation and oxidative stress, leaded to the embryo toxicity and organs deformity, and affected the cardiovascular, nervous and locomotor system development.