IMR Press / FBE / Volume 3 / Issue 2 / DOI: 10.2741/E262

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Sodium thiosulfate exposure disrupts in vitro and in vivo heart development

Yi Cui1,2,3Liyong Liu4Hongfei Xia1,2,3Zhongji Han1,2,3Yi Hu1,2,3Xu Ma1,2,3,*
Show Less
1 Reproductive and Genetic Center of National Research Institute for Family Planning, Beijing, 100081, China
2 WHO Collaborative Center for Research in Human Reproduction, Beijing, 100081, China
3 Department of Genetics, Graduate school of peking union medical college, Beijing, 100005, China
4 North China Coal Medical College, Tangshan, China
Front. Biosci. (Elite Ed) 2011, 3(2), 469–475; https://doi.org/10.2741/E262
Published: 1 January 2011
Abstract

It is well-known that the majority of malformations found in the human population is based on complex gene-environment interactions. As an industrial chemical sodium thiosulfate (STS) is used heavily in many industries. Nevertheless, there is little known about the effects of STS on embryo development. In the present study, we have investigated the effects of STS on cardiac development in rat cardiomyocyte H9C2 cell line and chick embryos. As determined by MTT assays, the proliferation of H9C2 cells was inhibited by STS in a dose-dependent manner. Fertilized eggs injected via the yolk sac with STS at Hamburger-Hamilton (HH) stages 6, 9 and 12 showed significantly increased cardiotoxicity at HH stage 18, including cardiomyocyte apoptosis and animal mortality. Western blot analysis showed that STS significantly affected the expression of the apoptosis-related genes bcl-2, bax, and caspase-3 in a dose-dependent manner in the H9C2 cell line and in chick embryos. Dysregulation of apoptosis was correlated with embryonic heart malformations. Thus, STS may be a potent cardiac teratogen during embryo development.

Share
Back to top