Schmidt K L, Milner K, Hilburn P J, Schmidt W A
Teratology. 1983 Aug;28(1):131-44. doi: 10.1002/tera.1420280116.
The histological and cytological basis of trypan blue-induced ocular defects were studied using scanning and transmission electron microscopy. Microphthalmic and anophthalmic eyes of 16-day rat fetuses were utilized from dams exposed to a teratogenic dose of trypan blue. Retinal and lenticular anlagen were specifically examined for architectural and cellular changes. Nearly all severely abnormal eyes showed no evidence of retina development: Of 41 such eyes, only two retinal rudiments were observed. Those eyes with mild microphthalmia always demonstrated retinae although architectural changes were present. In every abnormal eye, some degree of lenticular morphogenesis was always present. Lenses were small, displaced in the eye field, and arrested at the lens vesicle stage. Lens cells were markedly undifferentiated and thus lacked most of the cytological features normally present at this developmental stage. Neither retinal nor lenticular rudiments were necrotic despite major architectural and cytological disturbances. The data offer three conclusions: First, the absence of necrosis suggests that trypan blue causes developmental arrest in this eye model; second, absence of retinae is most likely due to primary failure of optic vesicle development; third, lack of lens differentiation is attributed to absence of the retina, the primary lens inducer.
利用扫描电子显微镜和透射电子显微镜研究了锥虫蓝诱导的眼部缺陷的组织学和细胞学基础。从暴露于致畸剂量锥虫蓝的母鼠体内获取16天龄大鼠胎儿的小眼和无眼。特别检查了视网膜和晶状体原基的结构和细胞变化。几乎所有严重异常的眼睛都没有视网膜发育的迹象:在41只这样的眼睛中,仅观察到两个视网膜原基。那些轻度小眼的眼睛总是有视网膜,尽管存在结构变化。在每只异常眼睛中,总是存在一定程度的晶状体形态发生。晶状体很小,在眼内移位,并停滞在晶状体泡阶段。晶状体细胞明显未分化,因此缺乏这个发育阶段通常存在的大多数细胞学特征。尽管存在主要的结构和细胞学紊乱,但视网膜和晶状体原基均未坏死。这些数据提供了三个结论:第一,没有坏死表明锥虫蓝在这个眼模型中导致发育停滞;第二,没有视网膜很可能是由于视泡发育的原发性失败;第三,晶状体缺乏分化归因于缺乏视网膜,即主要的晶状体诱导物。