首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Increased mitochondrial DNA deletion in the brain of SAMP8, a mouse model for spontaneous oxidative stress brain.
【24h】

Increased mitochondrial DNA deletion in the brain of SAMP8, a mouse model for spontaneous oxidative stress brain.

机译:SAMP8(自发性氧化应激脑的小鼠模型)的大脑中线粒体DNA缺失增加。

获取原文
获取原文并翻译 | 示例
           

摘要

Oxidative stress is considered to be closely correlated with degenerative brain abnormalities. In this study, the plausibility of a SAMP8 strain mouse showing memory deterioration and short life span as an oxidative stress brain model was evaluated. Mitochondrial DNA deletions were detected using polymerase chain reaction (PCR) as cumulative spontaneous oxidative stress. In the 4-8-week-old SAMP8 brain, multiple mitochondrial DNA (mtDNA) deletions were already found and the contents were significantly higher than those of SAMR1 or ddY controls. Enzyme activity studies indicated that electron transport was disturbed at the lower site of the chain and the electronegativity of the upper site might be increased, a cause of radical production and therefore oxidative stress.
机译:氧化应激被认为与变性脑异常密切相关。在这项研究中,评估了SAMP8品系小鼠作为氧化应激脑模型表现出记忆力下降和寿命短的真实性。使用聚合酶链反应(PCR)检测线粒体DNA缺失作为累积的自发氧化应激。在4-8周大的SAMP8脑中,已经发现了多个线粒体DNA(mtDNA)缺失,并且其含量明显高于SAMR1或ddY对照。酶活性研究表明,在链的下部位点电子传输受到干扰,上部位点的电负性可能增加,这是自由基产生的原因,因此也是氧化应激的原因。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号