Cultured murine dermal fibroblast-like cells from senescence-accelerated mice as in vitro models for higher oxidative stress due to mitochondrial alterations
Cultured murine dermal fibroblast-like cells from senescence-accelerated mice as in vitro models for higher oxidative stress due to mitochondrial alterations
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DOI：
10.1093/gerona/60.9.1087
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发表时间：
2005-09-01
影响因子：
5.1
通讯作者：
Hosokawa, M
中科院分区：
文献类型：
--
作者：
Chiba, Y;Yamashita, Y;Hosokawa, M
0加速衰老小鼠是一种加速衰老的模型。氧化应激状态以及与年龄相关的疾病。我们研究了从加速衰老倾向的SAMP 11小鼠培养的成纤维细胞是否可以用作衰老中氧化应激的体外模型。二氯荧光素和氢乙啶测定表明，SAMP 11小鼠的细胞产生更多的活性氧比加速衰老的抗SAMR 1小鼠的细胞。这些差异不是由于抗氧化剂的诱导缺陷。双标记与hydroethidine和MitoTracker绿色显示，大部分的活性氧在线粒体内产生。壬基吖啶橙子和JC-1检测显示，在SAMP 11细胞中，线粒体的质量增加，尤其是那些具有低膜电位的线粒体。超微结构观察发现，随着培养时间的延长，SAMP 11细胞线粒体数量增多，形态发生退行性改变。这些结果表明，来自SAMP 11小鼠的细胞是由于线粒体功能障碍而导致的体外自发性较高氧化应激的有用模型。
0The senescence-accelerated mouse is a model for senescence acceleration. a hiaher oxidative stress status, and age-associated disorders. We studied whether fibroblasts cultured from accelerated senescence-prone SAMP11 mice could be used as in vitro models for oxidative stress in senescence. Dichlorofluorescein and hydroethidine assays demonstrated that cells from SAMP11 mice produced more reactive oxygen species than did cells from accelerated senescence-resistant SAMR1 mice. These differences were not due to the defective induction of antioxidants. Double labeling with hydroethidine and MitoTracker Green revealed that most of the reactive oxygen species were generated within the mitochondria. Nonyl acridine orange and JC-1 assays showed an increase in the mass of the mitochondria, especially those with low membrane potential, in SAMP11 cells. Ultrastructurally, mitochondria with degenerative morphology were increased in SAMP11 cells with longer culture periods. These results suggest that cells from SAMP11 mice are useful models for spontaneous higher oxidative stress in vitro due to dysfunctional mitochondria.