Wada E, Takenawa T, Tsumita T
Biochim Biophys Acta. 1979 Jun 13;554(1):148-55. doi: 10.1016/0005-2736(79)90014-2.
The myo-inositol uptake system was studied in lenses of normal and hereditary cataract mouse. The normal mouse was able to accumulate myo-inositol continuously from medium and keep it in a high concentration. The specific myo-inositol uptake was dependent on temperature and it decreased in Ca(2+)-free medium. In contrast, specific uptake of myo-inositol reached a plateau after 15 min in the cataract mouse lens although initial incorporation was more rapid than that in normal mouse lens. This uptake system was not affected by temperature or Ca(2+) in the medium. The rate of myo-inositol efflux into the medium was more rapid in the cataract lens than that of the normal lens. It was shown that the low level of myo-inositol in the lens of hereditary cataract mouse was due to the defect of myo-inositol transport system and the enhanced efflux rate. These results suggest a dysfunction of the lens membrane.
对正常小鼠和遗传性白内障小鼠的晶状体中的肌醇摄取系统进行了研究。正常小鼠能够持续从培养基中积累肌醇并将其保持在高浓度。肌醇的特异性摄取取决于温度，在无钙培养基中会降低。相比之下，尽管白内障小鼠晶状体中肌醇的初始掺入比正常小鼠晶状体更快，但15分钟后其特异性摄取达到了平台期。这种摄取系统不受培养基中温度或钙离子的影响。白内障晶状体中肌醇向培养基中的流出速率比正常晶状体更快。结果表明，遗传性白内障小鼠晶状体中肌醇水平较低是由于肌醇转运系统缺陷和流出速率增加所致。这些结果提示晶状体膜功能障碍。
