氯化甲基汞激发程序性细胞死亡与胚胎神经系统发育的关系探讨

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。

Relation between Methylmercury Chloride induced Programmed Cell Death and the Development of Nervous System in Rats

The study was designed to reveal the role of programmed cell death (PCD, or apoptosis) induced by methylmercury chloride (MMC) in SD rat embryos, wish TdT mediated dUTP nick end labeling (TUNEL), Nile blue sulfate (NBS) vital stailing electron microscopy (SEM) and in vivo teratogenic methods (TEM). Pregnant rats were intraperitoneally injected at gestation day 9 5 with doses of 0, 0 2, 0 4, 0 8, 1 6 and 3 2 mg/kg MMC and killed at 11 5 day later. Results showed that the PCD of embryonic nervous system was apparently dose dependent with MMC during rat head fold stage.Observations under SEM and TEM showed that MMC caused pathologic changes of epithelia and organellae in embryonic brain such as atrophied or decreased microvilli, cavernous damages and mitochondrial swelling and so on.Though MMC could result in developmental anomalies of embryonic brain and other organs, the main defect was open neural tube. The experiment study suggested that over PCD may be one of the teratogenic mechanisms of MMC on rat embryos, developing brain in particular.