Wang Yun-ying, Sui Ke-xu, Li Hong, Ma Hai-yan
Department of Medical Genetics, Affiliated Qingdao Municipal Hospital of Qingdao University Medical College, Qingdao, Shandong 266011, People's Republic of China.
Reprod Toxicol. 2009 Apr;27(2):190-5. doi: 10.1016/j.reprotox.2008.12.006. Epub 2008 Dec 30.
The present study was designed to investigate the toxicity of lead exposure on the placenta at different dosages and the relationship with placental expression of NF-kappaB. A total of 67 unrelated Han Chinese pregnant women and 108 Wistar rats were included in this study. The rats were randomly divided into four groups for consumption of water with or without 0.025% lead acetate during various gestational periods; blood samples and placenta were harvested for analysis. Blood lead content was determined by atomic absorption spectrophotometry. Placental NF-kappaB expression was evaluated by immunohistochemistry. Placental cytoarchitecture was examined by histopathology and electronic microscopy. Fetal body weight, body length and placental weight was significantly lower (p<0.05) in the lead-exposed rats compared to controls. Maternal blood lead levels in the rats negatively correlated with placental weight (r=0.652, p<0.01). Rat placenta showed focal necrosis in the decidua with trophoblast degeneration and fibrin deposition. Mitochondria were swollen and decreased in number, rough endoplasmic reticula were distended and ribosomal number on membranes decreased. In the human placenta, we did not find abnormal cytoarchitecture. On the other hand, placental expression of NF-kappaB in lead-exposed rats was significantly higher than that in controls and the expression of NF-kappaB in human placenta was positively correlated with maternal blood lead levels (r=0.663, p<0.01). These findings suggest that lead exposure at various gestational periods produce varied effects, with NF-kappaB activation following lead exposure. Injury to cytoplasmic organelles may interfere with the nutrition and oxygen exchange between mother and fetus, which may be contribute to abnormal pregnancy outcomes.
本研究旨在探讨不同剂量铅暴露对胎盘的毒性作用及其与胎盘核因子-κB(NF-κB)表达的关系。本研究共纳入67名无亲缘关系的汉族孕妇和108只Wistar大鼠。将大鼠随机分为四组,在不同孕期饮用含或不含0.025%醋酸铅的水;采集血样和胎盘进行分析。采用原子吸收分光光度法测定血铅含量。通过免疫组织化学法评估胎盘NF-κB表达。通过组织病理学和电子显微镜检查胎盘细胞结构。与对照组相比,铅暴露大鼠的胎儿体重、体长和胎盘重量显著降低(p<0.05)。大鼠母体血铅水平与胎盘重量呈负相关(r=0.652,p<0.01)。大鼠胎盘蜕膜出现局灶性坏死,伴有滋养层变性和纤维蛋白沉积。线粒体肿胀且数量减少,粗面内质网扩张,膜上核糖体数量减少。在人胎盘中,我们未发现细胞结构异常。另一方面,铅暴露大鼠胎盘NF-κB表达显著高于对照组,人胎盘NF-κB表达与母体血铅水平呈正相关(r=0.663,p<0.01)。这些发现表明,不同孕期的铅暴露会产生不同影响,铅暴露后会激活NF-κB。细胞质细胞器损伤可能会干扰母体与胎儿之间的营养和氧气交换,这可能导致异常妊娠结局。