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What makes some rats live so long? The mitochondrial contribution to longevity through balance of mitochondrial dynamics and mtDNA content

机译：是什么让一些老鼠活得这么久？通过平衡线粒体动力学和线粒体DNA含量线粒体对长寿的贡献

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Extremely interesting for aging research are those individuals able to reach older ages still with functions similar to those of younger counterparts. We examined liver samples from ad libitum-fed old (28-month-old, AL-28) and ad libitum-fed very old (32-month-old, AL-32) rats for a number of markers, relevant for mitochondrial functionality and mitochondrial DNA (mtDNA) content. As for the mtDNA content and the protein amounts of the citrate synthase and the antioxidant peroxiredoxin III there were no significant changes in the AL-32 animals. No significant longevity-related change was found for TFAM amount, but a 50% reduction in the amount of the Lon protease, responsible for turnover of TFAM inside mitochondria, characterized the AL-32 rats. No longevity-related change was observed also for the amounts of the mtDNA repair enzymes OGG1 and APE1, whereas the intra-mitochondrial amount of the cytochrome c protein showed a 50% increase in the AL-32 rats, indicating a likely reduced initiation of the intrinsic apoptotic pathway. Totally unexpected was the doubling of two proteins, very relevant for mitochondrial dynamics, namely MFN2 and DRP1, in the AL-32 rats. This prompted us to the calculation of all individual fusion indexes that grouped together in the AL-32 rats, while in the AL-28 animals were very different. We found a strong positive correlation between the fusion indexes and the respective mtDNA contents in two AL-28 and four AL-32 rats. This supports the idea that the limited prevalence of fusion above a still active fission should have ensured a functional mitochondrial network and should have led to a quite narrow range of high mtDNA contents, likely the best-suitable for extended longevity. Our findings strongly suggest that, among the multiple causes leading to the longevity of the AL-32 rats, the maintenance of an adult-like balance of mitochondrial dynamics seems to be very relevant for the regulation of mtDNA content and functionality.
机译：对于衰老研究而言，最有趣的是那些能够达到更高年龄但仍具有与年轻同行相似的功能的人。我们检查了随意采食的老鼠（28个月大，AL-28）和随意采食的老鼠（32个月大，AL-32）大鼠的肝样品中的许多与线粒体功能有关的标志物和线粒体DNA（mtDNA）含量。至于柠檬酸合酶和抗氧化剂过氧化物酶Ⅲ的mtDNA含量和蛋白质量，在AL-32动物中没有显着变化。没有发现长寿相关的TFAM量有显着变化，但AL-32大鼠的特征是线粒体内TFAM转换的Lon蛋白酶量减少了50％。 mtDNA修复酶OGG1和APE1的量也没有观察到与寿命有关的变化，而AL-32大鼠的线粒体内细胞色素c蛋白的量显示增加了50％，这表明它的启动可能减少了。固有的凋亡途径。完全出乎意料的是，AL-32大鼠中与线粒体动力学非常相关的两种蛋白质加倍，即MFN2和DRP1。这促使我们计算在AL-32大鼠中归为一组的所有单个融合指数，而在AL-28动物中则完全不同。我们发现两只AL-28和四只AL-32大鼠的融合指数与各自的mtDNA含量之间存在很强的正相关。这支持了这样的想法，即仍然活跃的裂变上方的融合发生率有限，应确保线粒体网络功能正常，并应导致较高的mtDNA含量范围很窄，可能最适合延长寿命。我们的发现有力地表明，在导致AL-32大鼠寿命延长的多种原因中，线粒体动力学的成年状维持似乎与mtDNA含量和功能的调节非常相关。

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