Embryonic development toxicity of selenite in zebrafish (Danio rerio) and prevention with folic acid
- Authors
- Ma, Y., Wu, M., Li, D., Li, X.Q., Li, P., Zhao, J., Luo, M.N., Guo, C.L., Lu, C.L., and Ma, X.
- ID
- ZDB-PUB-120517-3
- Date
- 2012
- Source
- Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 508: 2854-2863 (Journal)
- Registered Authors
- Keywords
- selenite embryotoxicity, zebrafish, heart development, neural development, folic acid, DNA methylation
- MeSH Terms
-
- Animals
- DNA Methylation
- Embryo, Nonmammalian/drug effects*
- Folic Acid/pharmacology*
- Heart/drug effects
- Heart/embryology
- Sodium Selenite/toxicity*
- Teratogens/toxicity*
- Zebrafish/embryology*
- PubMed
- 22583652 Full text @ Food Chem. Toxicol.
Selenium (Se) is an essential micronutrient, but also a potential toxin, which may be absorbed in excess. Relatively little is known about selenium embryotoxicity in zebrafish. In this study, we evaluated the effect of selenite exposure in zebrafish embryos. Selenite treatment decreased survival and resulted in abnormal development in a dose- and time-dependent manner. We observed irregular growth of neurons in selenite treated embryos, characterized by the absence of neurons in the brain, trunk and tail. Selenite exposure also induced defects in heart function, such as bradycardia and cardiac dysplasia with irregular and smaller chamber shape. In addition, selenite exposure caused ectopic cell proliferation, apoptosis, and a change in the pattern of DNA methylation. Our results suggested that supplementation with folic acid (FA) ameliorated the cardiac and neural defects in selenite-treated embryos. In conclusion, we demonstrated that selenite exposure caused cardiac and neural defects in zebrafish embryos and that folic acid protected against this embryotoxicity. It will give insight into the risk assessment and prevention of Se-mediated embryotoxicity.