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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Impairment of lon-induced protection against the accumulation of oxidized proteins in senescent wi-38 fibroblasts.
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Impairment of lon-induced protection against the accumulation of oxidized proteins in senescent wi-38 fibroblasts.

机译：lon诱导的针对衰老的wi-38成纤维细胞中氧化蛋白积累的保护作用受损。

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Oxidative damage to mitochondrial proteins is thought to contribute to the aging process, but the Lon protease normally degrades such proteins. In early-passage WI-38 human lung fibroblasts, Lon expression is rapidly induced during H(2)O(2) stress, which prevents the accumulation of oxidized proteins and protects cell viability. In contrast, middle passage cells exhibit only sluggish induction of Lon expression in oxidative stress, and oxidized proteins initially accumulate. Late-passage, or senescent, cells have low basal levels of Lon and high levels of accumulated oxidized proteins; in response to oxidative stress, they fail to induce Lon expression and exhibit continually increasing accumulation of oxidized proteins. Senescent cells separated into two populations, one exhibiting normal mitochondrial mass and a second displaying significant loss of mitochondria; both populations had diminished mitochondrial transmembrane potential. These senescent changes are similar to the effects of Lon silencing in young cells. We suggest that loss of Lon stress inducibility is part of a pattern of diminishing stress adaptability that predisposes cells to senescence.
机译：线粒体蛋白的氧化损伤被认为是导致衰老的原因，但Lon蛋白酶通常会降解此类蛋白。在早期传代的WI-38人肺成纤维细胞中，Lon表达在H（2）O（2）压力过程中被迅速诱导，这防止了氧化蛋白的积累并保护了细胞活力。相比之下，中层传代细胞在氧化应激中仅表现出对Lon表达的缓慢诱导，并且最初积累了氧化蛋白。晚期传代或衰老的细胞具有较低的基础Lon水平和高水平的累积氧化蛋白。响应氧化应激，它们不能诱导Lon表达，并表现出不断增加的氧化蛋白积累。衰老细胞分为两个种群，一个种群显示正常的线粒体质量，另一个种群显示出明显的线粒体损失。两种种群均降低了线粒体跨膜电位。这些衰老变化类似于年轻细胞中Lon沉默的影响。我们建议失去Lon应激诱导力是减少压力适应能力模式的一部分，这种模式会使细胞易于衰老。

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