Shirai S
Department of Ophthalmology, Nagoya City University Medical School.
Nippon Ganka Gakkai Zasshi. 1991 Dec;95(12):1206-37.
Experimental teratology in mice was studied to clarify the developmental mechanisms of congenital eye abnormalities. Pregnant Jcl: ICR mice were treated intraperitoneally with ochratoxin A on day 7 of pregnancy. The offspring were grossly observed on day 9, 10, 11, 12, 13, 14, 16 or 18 of gestation, or at the second or fourth week after birth. Then, the eyes were histologically examined in serial sections. Mother mice were injected with ochratoxin A on day 8, 9, 10 or 11 of pregnancy, and the eyes of fetuses were examined on day 16 of gestation to determine the critical periods for the congenital eye abnormalities. Pregnant C57BL/6NJcl mice were also given an intraperitoneal injection of ochratoxin A on day 7 of pregnancy, and the eyes of offspring were observed grossly and histologically on day 16 or 18 of gestation, or at the second or fourth week after birth. Fetal and postnatal eyes showed various kinds and degrees of developmental abnormalities histologically. They included anophthalmia, microphthalmia, aphakia, mesenchymal dysgenesis of the anterior segment, faulty separation of the lens vesicle, developmental abnormalities of the vitreous, faulty closure of the embryonic fissure, retinal rosette formation and aberrant optic nerve fiber. Since anophthalmia, microphthalmia and aphakia caused by the developmental disturbances of the optic and lens vesicles were not established in the fetuses whose mothers were treated with ochratoxin A after day 9 of pregnancy, the critical periods for these abnormalities were considered to be on day 8 of gestation or earlier. Mesenchymal dysgenesis of the anterior segment, faulty separation of the lens vesicle and developmental abnormalities of the vitreous were frequently observed in the fetuses whose mothers were injected with ochratoxin A on day 7, 8 or 9 of pregnancy. It was considered that there was a correlation between the critical periods for these three abnormalities and the stage of the neural crest cell migration around the optic vesicle. Mesenchymal dysgenesis of the anterior segment observed in mice corresponded to the Axenfeld-Rieger syndrome or Peters' anomaly encountered clinically. Processes of production of these abnormalities based on the faulty migration of the neural crest cells which form the ocular anterior segment were demonstrated.(ABSTRACT TRUNCATED AT 400 WORDS)
为阐明先天性眼部异常的发育机制，对小鼠进行了实验性致畸学研究。怀孕的Jcl:ICR小鼠在妊娠第7天腹腔注射赭曲霉毒素A。在妊娠第9、10、11、12、13、14、16或18天，或出生后第二周或第四周对后代进行大体观察。然后，对眼睛进行连续切片的组织学检查。在妊娠第8、9、10或11天给母鼠注射赭曲霉毒素A，并在妊娠第16天检查胎儿的眼睛，以确定先天性眼部异常的关键时期。怀孕的C57BL/6NJcl小鼠也在妊娠第7天腹腔注射赭曲霉毒素A，并在妊娠第16或18天，或出生后第二周或第四周对后代的眼睛进行大体和组织学观察。胎儿和出生后的眼睛在组织学上表现出各种类型和程度的发育异常。包括无眼、小眼、无晶状体、前段间充质发育不全、晶状体泡分离异常、玻璃体发育异常、胚胎裂闭合异常、视网膜玫瑰花结形成和视神经纤维异常。由于在妊娠第9天之后用赭曲霉毒素A处理过的母鼠所生的胎儿中，未出现由视泡和晶状体泡发育障碍引起的无眼、小眼和无晶状体，因此这些异常的关键时期被认为是在妊娠第8天或更早。在妊娠第7、8或9天给母鼠注射赭曲霉毒素A的胎儿中，经常观察到前段间充质发育不全、晶状体泡分离异常和玻璃体发育异常。认为这三种异常的关键时期与视泡周围神经嵴细胞迁移阶段之间存在相关性。小鼠中观察到的前段间充质发育不全与临床上遇到的Axenfeld-Rieger综合征或彼得斯异常相对应。基于形成眼前段的神经嵴细胞迁移错误产生这些异常的过程得到了证实。（摘要截于400字）
