衰老小鼠线粒体DNA缺失突变的研究  

Study on mitochondrial DNA deletion in aging mice

作　　者：陈姝[1] 何蕴韶[2] 程钢[2] 高劲松[2] 

机构地区：[1]广东省佛山市第一人民医院临床医学研究所,广东佛山528000 [2]中山大学达安基因诊断中心,广东广州510080

出　　处：《分子诊断与治疗杂志》2009年第3期168-171,共4页Journal of Molecular Diagnostics and Therapy

摘　　要：目的测定不同年龄组及D-半乳糖诱导的衰老小鼠线粒体DNA(mtDNA)缺失突变,探讨mtDNA缺失突变与衰老的关系。方法用聚合酶链反应技术和琼脂糖凝胶电泳检测mtDNA缺失片段,用密度扫描技术对扩增片段进行相对定量。缺失片段构建质粒后,直接测序进行鉴定。结果全部小鼠的肝、脑与海马组织内均存在4239bp的mtDNA缺失片段。老年鼠肝、脑与海马组织内mtDNA缺失的比例较青幼年鼠明显增加(P<均0.01)。衰老模型鼠不同组织mtDNA缺失的相对百分含量均明显高于实验对照组(P均<0.01),肝组织中mtDNA缺失的比例较大脑皮层和海马组织更高。结论4239bp的mtDNA缺失片段普遍存在于小鼠中,与增龄和衰老相关,可作为衰老的一种分子生物标志。Objective To measure mitochondrial DNA(mtDNA)deletion from in different age groups mice and senile mice induced by D-galactose,and study the relevance between the mtDNA deletion and the aging.Methods Polymerase chain reaction technique and electrophoresis were used to examine the fragment deletion of mtDNA.Quantitation of relative band densities was performed using densitometry scanning techniques.The deletion was identified by direct sequencing analysis.Results A 4 239 bp mtDNA deletion was present in liver,cerebral cortex and hippocampus tissues from all of mice.The relative percentage contents of mtDNA deletion in various tissues increased significantly in old mice compared with young and adult mice(P<0.01,respectively).The deletion of mtDNA was significantly higher in senile model mice induced by D-galactose than those of NS group mice(P<0.01,respectively).Deletion was more abundant in liver than in cerebral cortex and hippocampus.Conclusion The results indicated that such 4 239 bp mtDNA deletion was a common deletion,which was more causally linked to senescence and could be a kind of molecular biomarker of senescence.

关 键 词：衰老 D-半乳糖 线粒体DNA 缺失 

分 类 号：R285.5[医药卫生—中药学]