Cook C S, Nowotny A Z, Sulik K K
Department of Anatomy, School of Medicine, University of North Carolina, Chapel Hill 27514.
Arch Ophthalmol. 1987 Nov;105(11):1576-81. doi: 10.1001/archopht.1987.01060110122045.
Acute maternal ethanol administration on gestational day 7 (gastrulation stage) in C57Bl/6J mice results in a spectrum of ocular malformations. A deficiency in the anterior neural plate observable within 24 hours of exposure results in corresponding defects in the optic sulcus and subsequent optic vesicle. Deficiency in the size of the lens vesicle induced by a small optic vesicle is demonstrable as microphakia in older embryos. Delayed detachment of the lens vesicle from the surface ectoderm manifests in the live offspring as progressive corneal opacification and vascularization related to defects in corneal endothelium and Descemet's membrane. Anterior segment dysgenesis results in persistent iridocorneal adhesions, dyscoria, and abnormal formation of the anterior chamber. In contrast, ethanol exposure on day 8 of gestation did not result in eye malformations. Thus, it appears that many of the ocular abnormalities associated with fetal alcohol syndrome may result from an acute insult to the optic primordia during a very specific period that corresponds to the third week after fertilization in the human.
在C57Bl/6J小鼠妊娠第7天（原肠胚形成期）急性给予母体乙醇会导致一系列眼部畸形。在暴露后24小时内可观察到前神经板缺陷，这会导致视沟及随后的视泡出现相应缺陷。由小视泡诱导的晶状体泡大小不足在较年长胚胎中表现为小晶状体。晶状体泡与表面外胚层延迟分离在存活后代中表现为与角膜内皮和Descemet膜缺陷相关的进行性角膜混浊和血管化。眼前节发育异常导致持续性虹膜角膜粘连、瞳孔异常和前房异常形成。相比之下，在妊娠第8天暴露于乙醇并未导致眼部畸形。因此，似乎许多与胎儿酒精综合征相关的眼部异常可能是由于在与人类受精后第三周相对应的非常特定时期对视原基的急性损伤所致。
