Ascorbic acid inhibits ROS production, NF-kappa B activation and prevents ethanol-induced growth retardation and microencephaly.
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.
Peng
Ying
Y
Department of Neurology, The Second Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China, 510120. ypeng@hkucc.hku.hk
Kwok
K H H
KH
Yang
Pai-Hao
PH
Ng
Samuel S M
SS
Liu
Jie
J
Wong
O G
OG
He
Ming-Liang
ML
Kung
Hsiang-Fu
HF
Lin
Marie C M
MC
D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D000431:Ethanol / Q000037:antagonists & inhibitors / Q000633:toxicity*; D005317:Fetal Growth Retardation / Q000139:chemically induced / Q000517:prevention & control*; D008831:Microcephaly / Q000139:chemically induced / Q000517:prevention & control*; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors* / Q000378:metabolism; D014982:Xenopus laevis
D016328:NF-kappa B; D017382:Reactive Oxygen Species; D000431:Ethanol; D001205:Ascorbic Acid