这些数据表明晶状体蛋白的非酶糖基化可能会导致白内障。

These data suggest that nonenzymatic glycosylation of lens crystallins may contribute to cataract formation.

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两者协同作用能有效地修复晶状体蛋白质和酶的巯基，维持晶状体的功能。

The two enzymes may work synergistically to repair thiols in lens proteins and enzymes and maintain the function of the lens effectively.

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目的：研究半乳糖诱导白内障大鼠异常晶状体蛋白x 36的出现及其与白内障形成的关系。

Objective: to study the abnormal crystalline protein X36 in cataract SD rat and to explore the relationship be-tween X36 and cataractogenesis.

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