Recent Published Articles

Prenatal cadmium exposure impairs neural tube closure via inducing excessive apoptosis in neuroepithelium


Jinlong Li , Shiyong Zhu , Xuenan Li , Xueyan Dai

DOI:10.1016/j.jes.2023.03.036

Received November 15, 2022,Revised , Accepted March 27, 2023, Available online April 05, 2023

Volume 36,2024,Pages 572-584

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.

Copyright © Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences. Published by Elsevier B.V. and Science Press. All rights reserved.京ICP备05002858号-3