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目的采用体内动物模型及体外晶状体温育模型探讨氧化应力损伤可能与半乳糖诱导的白内障相关。方法建立半乳糖白内障动物模型及温育在氧化应力下的晶状体模型，检查其ＭＤＡ、ＳＯＤ、ＧＳＨ－ｐｘ、ＣＡＴ、ＧＳＨ、ＶｉｔａｍｉｎＥ、ＶｉｔａｍｉｎＣ的水平。结果对整体动物晶状体形态学及其分期的观察表明顺序出现囊泡前期，囊泡期，囊泡融合期，及皮质期，在动物模型晶状体中ＭＤＡ显著增高２５倍，然而ＧＳＨ、ＳＯＤ，可溶性蛋白分别减少３０％、５９％、２０％。在温育晶状体，ＭＤＡ显著增高３６倍，而ＧＳＨ、ＳＯＤ、ＧＳＦ－ｐｘ、ＣＡＴ、ＶｉｔａｍｉｎＥ和ＶｉｔａｍｉｎＣ分别下降８０％、２５％、６０％、６１％、１８％和６１％。结论半乳糖诱导的白内障除渗透损伤外，氧化应力也是重要的参与者
OBJECTIVE: To investigate the oxidative stress injury in galactose induced galactose induced by cataract in vivo using in vivo animal models and in vitro lens incubation models. Methods The animal models of galactose cataract and the model of lens under oxidative stress were established and the levels of MDA, SOD, GSH-px, CAT, GSH, Vitamin E and Vitamin C were examined. Results The observation of the morphology and staging of the whole animal lens showed that the sequence of pre-vesicle, vesicular phase, vesicular fusion phase and cortical phase increased significantly by 2.5 times in the animal model lens. However, GSH, SOD, Soluble protein decreased by 30%, 59%, 20% respectively. In the incubation of lens, MDA increased significantly by 3.6 times, while GSH, SOD, GSF-px, CAT, Vitamin E and Vitamin C decreased by 80%, 25%, 60%, 61%, 18% and 61% respectively. Conclusion Galactose-induced cataract is an important participant in addition to osmotic injury