Ascorbic acid inhibits ROS production, NF-kappa B activation and prevents ethanol-induced growth retardation and microencephaly

Neuropharmacology. 2005 Mar;48(3):426-34. doi: 10.1016/j.neuropharm.2004.10.018. Epub 2005 Jan 25.


In this study, we established an embryo model to study the effects of ethanol on fetal development. When embryos of Xenopus laevis (the African clawed frog) were exposed to ethanol, the resultant tadpoles had significantly reduced brain sizes (microencephaly) and retarded growth rates. These effects, similar to those observed in human fetal alcohol syndrome (FAS), were dose- and time-dependent. We further showed that the antioxidant ascorbic acid (vitamin C) could inhibit the ethanol-induced reactive oxygen species (ROS) production and NF-kappaB activation and protect the ethanol-treated embryos against microencephaly and growth retardation. These results suggest the involvement of NF-kappaB and oxidative stress in ethanol-mediated developmental defects, and the potential use of ascorbic acid as a new and effective protective agent for FAS.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ascorbic Acid / pharmacology*
  • Ascorbic Acid / therapeutic use
  • Ethanol / antagonists & inhibitors
  • Ethanol / toxicity*
  • Fetal Growth Retardation / chemically induced
  • Fetal Growth Retardation / prevention & control*
  • Microcephaly / chemically induced
  • Microcephaly / prevention & control*
  • NF-kappa B / antagonists & inhibitors*
  • NF-kappa B / metabolism
  • Reactive Oxygen Species / antagonists & inhibitors*
  • Reactive Oxygen Species / metabolism
  • Xenopus laevis


  • NF-kappa B
  • Reactive Oxygen Species
  • Ethanol
  • Ascorbic Acid