Brain lipid hydroperoxide level increases in senescence-accelerated mice at an early age

被引:49
作者
Yasui, F
Ishibashi, M
Matsugo, S
Kojo, S
Oomura, Y
Sasaki, K
机构
[1] Toyama Univ, Fac Engn, Div Bioinformat Engn, Toyama 9308555, Japan
[2] Yamanashi Univ, Interdisciplinary Grad Sch Med & Engn, Div Biotechnol, Kofu, Yamanashi 4008511, Japan
[3] Nara Womens Univ, Dept Food Sci & Nutr, Nara 6308263, Japan
[4] Kyushu Univ, Fac Med, Dept Physiol, Fukuoka 8128582, Japan
关键词
aging; senescence-accelerated mice; oxidative stress; lipid hydroperoxide level; brain; liver;
D O I
10.1016/S0304-3940(03)00827-9
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We previously reported that the levels of lipid hydroperoxides, one of oxidative stress markers, in the brain and peripheral organs such as liver, heart, and lung are significantly higher in senescence accelerated-prone 8 mice (SAMP8) than in their controls, senescence accelerated-resistant mice (SAMR1), at 3, 6, and/or 9 months of age. To ascertain the exact age at which the lipid hydroperoxide levels increase in SAMP8, we measured them in the brain and liver of SAMP8 and SAMR1 at both 1 and 2 months of age. At 1 month of age, there was no significant inter-strain difference in the levels in brain or liver. However, in SAMP8 both levels were significantly greater at 2 months of age than at I month of age, but no such difference was detected for SAMR1. The present results suggest that SAMP8 are exposed to elevated levels of oxidative stress from an early age (2 months old), and that this may be a cause of the senescence-related impairments and degeneration in the brain and peripheral tissues (such as liver, heart, and lung) seen in this strain. (C) 2003 Published by Elsevier Ireland Ltd.
引用
收藏
页码:66 / 68
页数:3
相关论文
共 16 条
  • [1] Alam ZI, 1997, J NEUROCHEM, V69, P1326
  • [2] Age-related cognitive deficits, impaired long-term potentiation and reduction in synaptic marker density in mice lacking the β-amyloid precursor protein
    Dawson, GR
    Seabrook, GR
    Zheng, H
    Smith, DW
    Graham, S
    O'Dowd, G
    Bowery, BJ
    Boyce, S
    Trumbauer, ME
    Chen, HY
    Van der Ploeg, LHT
    Sirinathsinghji, DJS
    [J]. NEUROSCIENCE, 1999, 90 (01) : 1 - 13
  • [3] The antioxidants α-lipoic acid and N-acetylcysteine reverse memory impairment and brain oxidative stress in aged SAMP8 mice
    Farr, SA
    Poon, HF
    Dogrukol-Ak, D
    Drake, J
    Banks, WA
    Eyerman, E
    Butterfield, DA
    Morley, JE
    [J]. JOURNAL OF NEUROCHEMISTRY, 2003, 84 (05) : 1173 - 1183
  • [4] Increased mitochondrial DNA deletion in the brain of SAMP8, a mouse model for spontaneous oxidative stress brain
    Fujibayashi, Y
    Yamamoto, S
    Waki, A
    Konishi, J
    Yonekura, Y
    [J]. NEUROSCIENCE LETTERS, 1998, 254 (02) : 109 - 112
  • [5] THE MEASUREMENT OF OXIDATIVE DAMAGE TO DNA BY HPLC AND GC/MS TECHNIQUES
    HALLIWELL, B
    DIZDAROGLU, M
    [J]. FREE RADICAL RESEARCH COMMUNICATIONS, 1992, 16 (02): : 75 - 87
  • [6] Korolainen MA, 2002, ELECTROPHORESIS, V23, P3428, DOI 10.1002/1522-2683(200210)23:19<3428::AID-ELPS3428>3.0.CO
  • [7] 2-5
  • [8] LEVINE RL, 1990, METHOD ENZYMOL, V186, P464
  • [9] Lyras L, 1998, J NEUROCHEM, V71, P302
  • [10] Age-dependent changes in lipid peroxide levels in peripheral organs, but not in brain, in senescence-accelerated mice
    Matsugo, S
    Kitagawa, T
    Minami, S
    Esashi, Y
    Oomura, Y
    Tokumaru, S
    Kojo, S
    Matsushima, K
    Sasaki, K
    [J]. NEUROSCIENCE LETTERS, 2000, 278 (1-2) : 105 - 108