Abstract：
Birth defects have become a public health concern. The hazardous environmental factors exposure to embryos could increase the risk of birth defects. Cadmium, a toxic environmental factor, can cross the placental barrier during pregnancy. Pregnant woman may be subjected to cadmium before taking precautionary protective actions. However, the link between birth defects and cadmium remains obscure. Cadmium exposure can induce excessive apoptosis in neuroepithelium during embryonic development progresses. Cadmium exposure activated the p53 via enhancing the adenosine 5\'-monophosphate (AMP)-activated protein kinase (AMPK) and reactive oxygen species\' (ROS) level. And cadmium decreases the level of Paired box 3 (Pax3) and murine double minute 2 (Mdm2), disrupting the process of p53 ubiquitylation. And p53 accumulation induced excessive apoptosis in neuroepithelium during embryonic development progresses. Excessive apoptosis led to the failure of neural tube closure. The study emphasizes that environmental materials may increase the health risk for embryos. Cadmium caused the failure of neural tube closure during early embryotic day. Pregnant women may be exposed by cadmium before taking precautionary protective actions, because of cadmium concentration-containing foods and environmental tobacco smoking. This suggests that prenatal cadmium exposure is a threatening risk factor for birth defects.
摘要：
出生缺陷已成为公共卫生问题。暴露于胚胎的有害环境因素会增加出生缺陷的风险。镉,有毒的环境因素，怀孕期间可以穿过胎盘屏障。孕妇在采取预防性保护措施之前可能会受到镉的影响。然而,出生缺陷和镉之间的联系仍然模糊。镉暴露可在胚胎发育过程中诱导神经上皮过度凋亡。镉暴露通过增强腺苷5'-单磷酸（AMP）激活的蛋白激酶（AMPK）和活性氧（ROS）水平激活p53。并且镉降低配对盒3（Pax3）和鼠双分钟2（Mdm2）的水平，破坏p53泛素化的过程。在胚胎发育过程中，p53的积累导致神经上皮过度凋亡。过度凋亡导致神经管闭合失败。该研究强调，环境材料可能会增加胚胎的健康风险。镉在胚胎早期导致神经管闭合失败。孕妇在采取预防性保护措施之前可能会接触镉，因为含镉浓度的食物和环境吸烟。这表明产前镉暴露是出生缺陷的威胁危险因素。
