ETHANOL-INDUCED TERATOGENESIS - FREE-RADICAL DAMAGE AS A POSSIBLE MECHANISM
ETHANOL-INDUCED TERATOGENESIS - FREE-RADICAL DAMAGE AS A POSSIBLE MECHANISM
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DOI：
10.1002/tera.1420520304
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发表时间：
1995-09-01
期刊：
影响因子：
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通讯作者：
SULIK, KK
中科院分区：
文献类型：
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作者：
KOTCH, LE;CHEN, SY;SULIK, KK
为了探讨乙醇致畸的自由基机制的可能性，将妊娠第8天的小鼠胚胎在全胚胎培养中暴露于致畸剂量的乙醇(500 mg%)或与抗氧化剂超氧化物歧化酶(SOD；300U/ml)联合作用6小时。为了随后的分析，一些胚胎在这6小时结束时被检查，而另一些胚胎被移到对照培养液中并培养一段额外的时间。酒精暴露导致胚胎超氧阴离子生成增加，脂质过氧化增加(如首次酒精暴露后6小时所示)，并导致细胞过度死亡(如首次暴露12小时后所述)。在总共36小时的培养后，注意到高发生率的畸形，包括63%的酒精暴露的胚胎前神经管未能闭合。乙醇诱导的超氧阴离子产生、脂质过氧化、细胞过度死亡和畸形发生在用超氧化物歧化酶共同处理的胚胎中被减少，这表明乙醇的致畸作用至少部分是由自由基损伤所介导的。(C)1995年Wiley-Liss公司
To investigate the possibility of a free radical mechanism for ethanol-induced teratogenesis, gestational day 8 mouse embryos were exposed for 6 hr in whole embryo culture to a teratogenic dosage of ethanol alone (500 mg%) or in conjunction with an antioxidant, superoxide dismutase (SOD; 300 U/ml). For subsequent analysis, some embryos were examined at the end of this 6-hr period, while others were removed to control medium and cultured for an additional time period. Ethanol exposure resulted in increased superoxide anion generation and increased lipid peroxidation (as noted 6 hr after initial ethanol exposure) and in excessive cell death (as noted 12 hr after initial exposure) in the embryos. Following a total of 36 hr in culture, a high incidence of malformation, including failure of the anterior neural tube to close in 63% of the ethanol-exposed embryos, was noted. The ethanol-induced superoxide anion generation, lipid peroxidation, excessive cell death, and dysmorphogenesis were diminished in embryos co-treated with SOD, suggesting that the teratogenicity of ethanol is mediated, at least in part, by free radical damage. (C) 1995 Wiley-Liss, Inc.