A higher oxidative status accelerates senescence and aggravates age-dependent disorders in SAMP strains of mice
A higher oxidative status accelerates senescence and aggravates age-dependent disorders in SAMP strains of mice
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DOI：
10.1016/s0047-6374(02)00091-x
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发表时间：
2002-11-01
影响因子：
5.3
通讯作者：
Hosokawa, M
中科院分区：
文献类型：
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作者：
Hosokawa, M
SAM品系小鼠实际上是一组相关的近交品系，由一系列SAMP（加速衰老倾向，短寿命）和SAMR（加速衰老抗性，长寿命）品系组成。与SAMR品系相比，SAMP品系小鼠显示出更加速的衰老过程、更短的寿命、以及与年龄相关的病理表型的更早发作和更快速的进展，这些病理表型类似于在人类中观察到的几种老年疾病，包括老年性骨质疏松症、退行性关节疾病、与年龄相关的学习和记忆缺陷、嗅球和前脑萎缩、老年性耳聋和视网膜萎缩、老年性淀粉样变性、免疫衰老、老年肺和主动脉弥漫性中层增厚。在SAMP品系小鼠中观察到的较高氧化应激部分由线粒体功能障碍引起，并且可能是细胞结构和功能的衰老加速和年龄依赖性改变（包括神经元细胞变性）的原因之一。在来自SAMP小鼠品系的分离的成纤维细胞样细胞的培养物的衰老/危机期间也观察到这种衰老加速，并且与过氧化状态相关。这些观察结果表明，SAM菌株是试图了解细胞和组织年龄依赖性变性及其恶化机制以及开发临床干预措施的有用工具。(C)2002爱思唯尔科学爱尔兰有限公司保留所有权利。
The SAM strain of mice is actually a group of related inbred strains consisting of series of SAMP (accelerated senescence-prone, short-lived) and SAMR (accelerated senescence-resistant, longer-lived) strains. Comparing with the SAMR strains, the SAMP strains of mice show a more accelerated senescence process, shorter lifespan, and an earlier onset and more rapid progress of age-associated pathological phenotypes similar to several geriatric disorders observed in humans, including senile osteoporosis, degenerative joint disease, age-related deficits in learning and memory, olfactory bulb and forebrain atrophy, presbycusis and retinal atrophy, senile amyloidosis, immuno senescence, senile lungs, and diffuse medial thickening of the aorta. The higher oxidative stress observed in the SAMP strains of mice are partly caused by mitochondrial dysfunction, and may be one cause of the senescence acceleration and age-dependent alterations in cell structure and function, including neuronal cell degeneration. This senescence acceleration is also observed during senescence/crisis in cultures of isolated fibroblast-like cells from SAMP strains of mice, and was associated with a hyperoxidative status. These observations suggest that the SAM strains are useful tools in the attempt to understand the mechanisms of age-dependent degeneration of cells and tissues, and their aggravation, and to develop clinical interventions. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.