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用ＴｄＴ介导脱氧核苷酸切口末端标记（ＴＵＮＥＬ）、尼罗兰活体染色、扫描和透射电镜及体内致畸试验等方法研究了氯化甲基汞（一次性腹腔注射剂量范围是０～３．２ｍｇ／ｋｇ）能否使神经胚形成期大鼠胚胎发生细胞凋亡亦称程序性细胞死亡（ＰＣＤ）及其ＰＣＤ对胚胎神经系统发育的影响。实验结果表明：随着甲基汞剂量的不断增高，胚胎脑组织ＰＣＤ检测阳性率亦显著增加，呈明显的剂量－反应关系；电镜下发现胚胎脑上皮细胞表面微绒毛数量减少和变短，细胞膜上出现大小不一的空洞样变，细胞器正常形态亦发生病理性改变，例如出现凋亡小体；甲基汞诱发脑发育异常的主要表现是神经管未闭。研究结果提示ＰＣＤ是甲基汞导致胚胎脑部畸形发生的重要机理之一。
Methylmercium chloride (0-3) was studied using TdT-mediated dendritic end labeling (TUNEL), Nile blue staining, scanning and transmission electron microscopy, and in vivo teratogenicity assays. 2mg / kg) can induce the apoptosis of embryonic cells in neurogenesis embryo, also known as programmed cell death (PCD) and PCD on embryonic nervous system development. The results showed that with the increase of methylmercury dose, the positive rate of PCD in embryonic brain tissue also increased significantly, showing a dose-response relationship. The number of microvilli on the surface of embryonic brain epithelial cells decreased and shortened under electron microscope. On the appearance of different sizes of holes, the normal morphology of organelles also occur pathological changes, such as the appearance of apoptotic bodies; methylmercury-induced brain dysplasia is the main manifestation of neural tube patent. The results suggest that PCD is one of the important mechanisms of methylmercury in embryonic brain deformity.