Ascorbic acid inhibits ROS production, NF-κB activation and prevents ethanol-induced growth retardation and microencephaly
Ascorbic acid inhibits ROS production, NF-κB activation and prevents ethanol-induced growth retardation and microencephaly
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DOI：
10.1016/j.neuropharm.2004.10.018
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发表时间：
2005-03-01
影响因子：
4.7
通讯作者：
Lin, MCM
中科院分区：
文献类型：
--
作者：
Peng, Y;Kwok, KHH;Lin, MCM
在本研究中，我们建立了一个胚胎模型来研究乙醇对胎儿发育的影响。当非洲爪蟾（非洲爪蟾）的胚胎暴露在乙醇中时，所产生的蝌蚪的大脑尺寸显着缩小（微脑畸形），生长速度减慢。这些效应与在人胎儿酒精综合征（FAS）中观察到的效应相似，具有剂量和时间依赖性。我们进一步表明，抗氧化剂抗坏血酸（维生素C）可以抑制乙醇诱导的活性氧（ROS）的产生和NF-κ B B的激活，并保护乙醇处理的胚胎，防止小脑畸形和生长迟缓。这些结果表明NF-κ B和氧化应激参与了乙醇介导的发育缺陷，以及抗坏血酸作为一种新的有效的FAS保护剂的潜在用途。(c)2004爱思唯尔有限公司保留所有权利。
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-kappa B activation and protect the ethanol-treated embryos against microencephaly and growth retardation. These results suggest the involvement of NF-kappa B and oxidative stress in ethanol-mediated developmental defects, and the potential use of ascorbic acid as a new and effective protective a-gent for FAS. (c) 2004 Elsevier Ltd. All rights reserved.