Beyer-Mears A, Bucci F A, Del Val M, Cruz E
Department of Physiology, UMD, New Jersey Medical School, Newark.
Pharmacology. 1989;39(1):59-68. doi: 10.1159/000138572.
The lens myo-inositol (MI) content is known to be depleted during initial cataractogenesis in both streptozocin (STZ)-induced diabetic and 50% galactose-maintained rats. The objective of this study is to establish whether dietary MI supplementation protects lens transparency, MI content and individual fiber cell ultrastructure is both model systems of sugar cataract. In the diabetic study, after induction with STZ, rats were immediately placed on normal chow supplemented with 2% MI for 14 weeks while additional age-matched control and diabetic rats remained untreated. Within 14 weeks, untreated diabetic rat lenses were totally opaque with undetectable MI content; MI was undetectable by 1 month. These opaque lenses were devoid of fiber cells and exhibited only acellular, amorphous cortical regions between 0 and 500 microns from the capsule. In contrast, 14-week, MI-treated diabetic rat lenses exhibited only cortical vacuolation indicative of initial cataractogenesis; MI content was 0.41 +/- 0.26 mumol/g wet weight of lens. Scanning electron micrographs indicated a granulated, acellular region subadjacent to the capsule and confirmed the presence of cortical fiber cells, approximately 100 microns from the capsule. In 50% galactose-maintained rats, daily administration of MI for 1 month was unable to prevent total opacification or reverse initial cataractogenesis indicating that in rapidly progressing galactose cataracts, MI was unable to protect lens transparency, MI content and cortical fiber ultrastructure. The combined results suggest that MI may exert a protective effect on the slowly developing diabetic cataract. Of the 2 models, the time course and polyol content in STZ diabetic lenses more closely correlate to the human diabetic lens which has a low activity of aldose reductase; therefore, it is possible that MI may exert a protective effect in human diabetic cataract.
已知在链脲佐菌素（STZ）诱导的糖尿病大鼠和50%半乳糖喂养的大鼠的早期白内障形成过程中，晶状体肌醇（MI）含量会减少。本研究的目的是确定在两种糖性白内障模型系统中，膳食补充MI是否能保护晶状体透明度、MI含量和单个纤维细胞超微结构。在糖尿病研究中，用STZ诱导后，大鼠立即被置于补充有2%MI的正常饲料中饲养14周，而另外的年龄匹配的对照大鼠和糖尿病大鼠不进行处理。在14周内，未处理的糖尿病大鼠晶状体完全混浊，MI含量无法检测到；1个月时MI就无法检测到了。这些混浊的晶状体没有纤维细胞，在距晶状体囊0至500微米之间仅表现为无细胞的、无定形的皮质区域。相比之下，经MI处理14周的糖尿病大鼠晶状体仅表现出皮质空泡形成，这是早期白内障形成的指征；MI含量为0.41±0.26微摩尔/克晶状体湿重。扫描电子显微镜照片显示，紧邻晶状体囊下方有一个颗粒状的无细胞区域，并证实了皮质纤维细胞的存在，距晶状体囊约100微米。在50%半乳糖喂养的大鼠中，每天给予MI 1个月无法预防完全混浊或逆转早期白内障形成，这表明在快速进展的半乳糖性白内障中，MI无法保护晶状体透明度、MI含量和皮质纤维超微结构。综合结果表明，MI可能对缓慢发展的糖尿病性白内障发挥保护作用。在这两种模型中，STZ糖尿病晶状体的时间进程和多元醇含量与醛糖还原酶活性低的人类糖尿病晶状体更密切相关；因此，MI有可能对人类糖尿病性白内障发挥保护作用。
