Murakami I, Kosano H, Ogihara-Umeda I, Nishigori H, Uga S, Ishikawa S
Faculty of Pharmaceutical Sciences, Teikyo University, Kanagawa, Japan.
Exp Eye Res. 1996 Dec;63(6):673-81. doi: 10.1006/exer.1996.0161.
In this paper various changes in glutathione level, which were influenced by balance of its synthesis, degradation, transport and utilization, were analysed in chick embryos administered with glucocorticoid (GC) or buthionine sulfoximine (BSO; an inhibitor of glutathione synthesis). When BSO (30 mumol egg-1) was administered twice to chick embryos on day 14 and 15, the GSH in both the lens and the liver decreased to 15-20% and 30-40% of the age-matched control level, respectively, between 24 and 48 hr after the second treatment, then began to recover. Although this decline in the GSH level in these tissues was greater and more prolonged in embryos treated with BSO than with GC, the former embryos maintained lens transparency even up to 144 hr by a visual examination. However, histological changes in the lens occurred after 96 hr and more significantly 144 hr after second administration of BSO. The changes mainly consisted of pale epithelial cells on the anterior peripheral surface of the lens, irregular height of the epithelial cells at the equator, clefts between the epithelium and the cortex and swelling of almost all the cortical fibers. These observations may suggest that BSO treatment could produce the beginning of a cataract. Embryos with GC-cataract revealed the following changes at 48 hr: loss of transparency, elevation of LPO (TBA-reacting substance) in the lens, the blood and the liver. These were not observed in BSO-treated embryos during the experimental period. The GC-cataract may well depend on the generation of LPO. BSO cataract, having a distinct mechanism compared to that caused by GC, develops more slowly in GSH-depleted lenses. The BSO-treated chick embryos will be a useful model to screen the risk factors which accelerate cataract formation.
在本文中，分析了在给予糖皮质激素（GC）或丁硫氨酸亚砜胺（BSO；谷胱甘肽合成抑制剂）的鸡胚中，受其合成、降解、转运和利用平衡影响的谷胱甘肽水平的各种变化。当在第14天和第15天对鸡胚两次给予BSO（30 μmol/蛋）时，在第二次处理后24至48小时之间，晶状体和肝脏中的谷胱甘肽分别降至同龄对照水平的15 - 20%和30 - 40%，然后开始恢复。尽管用BSO处理的胚胎中这些组织的谷胱甘肽水平下降比用GC处理的更大且更持久，但通过肉眼检查，前者胚胎直至144小时仍保持晶状体透明。然而，在第二次给予BSO后96小时，晶状体出现组织学变化，144小时时变化更明显。这些变化主要包括晶状体前周边表面的上皮细胞苍白、赤道处上皮细胞高度不规则、上皮与皮质之间的裂隙以及几乎所有皮质纤维肿胀。这些观察结果可能表明，BSO处理可引发白内障的起始。患有GC性白内障的胚胎在48小时时出现以下变化：透明度丧失、晶状体、血液和肝脏中脂质过氧化产物（TBA反应物质）升高。在实验期间，这些变化在BSO处理的胚胎中未观察到。GC性白内障很可能取决于脂质过氧化产物的产生。与GC引起的白内障相比，BSO性白内障具有独特的机制，在谷胱甘肽缺乏的晶状体中发展更慢。经BSO处理的鸡胚将成为筛选加速白内障形成风险因素的有用模型。
