【摘要】 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２５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３６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更多还原

【Abstract】 ObjectiveTo determine whether oxidative stress damage may be involved in galactose induced cataract in vivo and in vitro.MethodsA model of galactose induced cataract in SD rat was established by injecting 50% galactose(15 g/kg/d).An in vitro model was established by incubation of lenses in an oxygen free radical generation system.The levels of MDA,SOD,GSH px CAT,GSH,Vitamin E and C were examined.ResultsWe observed the morphology and pathology of lens opacity over time.The changes developed as follows:precystic vesicle,cystic vesicle,fusion cystic vesicles and cortical stage.In lenses of the animal model,the MDA was significantly increased 2 5 fold,but GSH,SOD,and water soluble protein were decreased by 30%,59% and 20%,respectively.In incubated lenses,the MDA was also significantly increased 3 6 fold,but GSH,SOD GSH PX,CAT,Vitamin E and C were decreased by 80%,25%,60%,61%,78% and 61%,respectively.ConclusionIt is important to determine the pathogenesis of galactose induced cataract;osmotic damage and oxidative stress appear to be involved.更多还原