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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >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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Cultured murine dermal fibroblast-like cells from senescence-accelerated mice as in vitro models for higher oxidative stress due to mitochondrial alterations.

机译：来自衰老加速小鼠的培养的鼠类真皮成纤维细胞样细胞，作为线粒体改变引起的较高氧化应激的体外模型。

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The senescence-accelerated mouse is a model for senescence acceleration, a higher 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.
机译：衰老加速小鼠是衰老加速，较高的氧化应激状态和与年龄相关的疾病的模型。我们研究了从易加速衰老的SAMP11小鼠培养的成纤维细胞是否可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，与来自加速抗衰老的SAMR1小鼠的细胞相比，来自SAMP11小鼠的细胞产生更多的活性氧。这些差异不是由于抗氧化剂的诱导缺陷所致。氢乙啶和MitoTracker Green的双重标记表明，大多数活性氧是在线粒体内产生的。壬基a啶橙和JC-1分析显示SAMP11细胞中线粒体的质量增加，尤其是膜电位较低的线粒体。超微结构，具有较长变性时间的SAMP11细胞中具有变性形态的线粒体增加。这些结果表明，由于线粒体功能异常，SAMP11小鼠的细胞是体外自发性较高氧化应激的有用模型。

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