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

被引:41
作者
Fujibayashi, Y [1 ]
Yamamoto, S
Waki, A
Konishi, J
Yonekura, Y
机构
[1] Fukui Med Univ, Biomed Imaging Res Ctr, Fukui, Japan
[2] Kyoto Univ, Grad Sch Pharmaceut Sci, Sakyo Ku, Kyoto 6068501, Japan
[3] Kyoto Univ, Grad Sch Med, Sakyo Ku, Kyoto 6068501, Japan
关键词
brain degeneration; oxidative stress; mitochondria; DNA deletion; senescence accelerated model mouse;
D O I
10.1016/S0304-3940(98)00667-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
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. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:109 / 112
页数:4
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