增龄对SAM小鼠脑线粒体DNA氧化损伤的影响  

Effect of aging on cerebral mitochondrial DNA oxidative damage of SAM mice

作　　者：田枫[1] 刘新文[1] 张宗玉[1] 

机构地区：[1]北京大学医学部生化与分子生物学系,北京大学衰老研究中心北京100083

出　　处：《中国老年学杂志》2005年第6期671-673,共3页Chinese Journal of Gerontology

基　　金：国家重点基础研究发展规划(G2000057001);国家自然科学基金项目(30371561)资助课题

摘　　要：目的探讨增龄对SAM小鼠脑线粒体DNA(mtDNA)缺失、活性氧自由基水平及脑组织总抗氧化能力的影响。方法SAMP/8和SAMR/1小鼠分别分为三组幼年组(0.5月龄)、青年组(2月龄)和老年组(12月龄)各6只。用PCR方法测定脑组织线粒体DNA缺失、用化学发光法测定总抗氧化能力及活性氧自由基。结果随增龄,SAMP/8小鼠脑组织线粒体DNA缺失增加,线粒体活性氧自由基水平升高,脑组织总抗氧化能力下降。结论随增龄,SAMP/8小鼠脑组织氧化损伤增加,可能是导致其记忆学习障碍的原因之一。Objective To explore the effect of aging on cerebral mitochondrial (mt) DNA deletions, active oxygen radical level and total anti-oxidization ability of brain tissues. Methods SAM-P/8 and SAM-R/1 mice were respectively divided into three groups, i.e. infant group (0.5 month-old), youth group (2 month-old) and senior group (12 month-old), with six mice in each group. Cerebral mtDNA deletions were determined by PCR while total anti-oxidization ability and active oxygen radical levels were detected by chemical luminescent method. Results With aging, mtDNA deletions in the brain tissue of SAM-P/8 mice increased with an elevated level of mt active oxygen radical level and lowered total anti-oxidization ability. Conclusions The increase of oxidative damage in brain tissue of SAM-P/8 mice with ageing might be one of the causes resulting in memory learning impediment.

关 键 词：线粒体DNA SAM小鼠 氧化损伤 

分 类 号：Q731[生物学—分子生物学]