D-半乳糖脑老化模型的脂质过氧化机理

Mechanism of lipid peroxidation in Dgalactoseinduced brain aging model

运用体内、体外相结合的方法观察了Ｄ－半乳糖（Ｄ－ｇａｌ）对脂质过氧化和蛋白质代谢的影响。结果表明：Ｄ－ｇａｌ使大鼠脑组织、家蝇头和培养大鼠神经细胞、人胚肺二倍体成纤维细胞（ＨＢＳ）均出现ＳＯＤ含量下降，ＭＤＡ和脂褐素（Ｌｉｐｏ）水平升高及大鼠全血中谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）水平降低等现象；此外，大鼠脑组织中总ＲＮＡ含量下降，可溶性蛋白减少，不可溶性蛋白增加，这些变化与老年对照相类似，也与黄嘌呤氧化酶－次黄嘌呤系统产生的Ｏ２结果一致。提示，在Ｄ－ｇａｌ的代谢过程中伴有活性氧自由基产生，以Ｏ２为主的自由基介导的脂质过氧化可能是该脑老化模型的主要原因。

おおhe effects of lipid peroxidation and protein metabolism induced by Dgalactose were investigated in vivo and in vitro.The levels of MDA,lipofuscin,SOD and GSHPx in rat ,house,cultured neruons and human fetal lung fibroblasts were studied respectively.The results showed that the levels MDA and lipofuscin were markedly increased,but SOD and GSHPx decreased,with that the total RNA and dissoluble protein reduced while undissoluble protein was increasde.These reasults were similar to those aged control and HypoxanthineXanthine reaction system(O-2),indicating that reactive oxyger species (ROS) especially (O-2).were generated in the course of Dgalatose metabolism,lipid peroxidation induced by ROS might be the cause of this brain aging model.