کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8264771 | 1534894 | 2010 | 4 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Perspectives on the mitochondrial etiology of replicative aging in yeast
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
In a now classical paper, Denham Harman suggested that free radicals produced during mitochondrial respiration cause cumulative oxidative damage, resulting in aging and age-related disorders and pathologies. Proponents of this hypothesis have focused their attention, not surprisingly, on mitochondria arguing that these organelles may serve as the biological clock for aging. Indeed, work on many models, including filamentous fungi, nematodes, and mammals have revealed that age-dependent reorganizations of the mitochondrial DNA (mtDNA) may play a central role in the aging of these organisms. Furthermore, genetic alterations of mitochondrial function may either shorten or extend life span. In this paper, we focus on the role of mitochondria in the replicative aging of yeast mother cells, whether this role of mitochondria is really a linked to altered ROS production and/or respiration, and highlight some important questions that remain to be answered.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Gerontology - Volume 45, Issues 7â8, August 2010, Pages 512-515
Journal: Experimental Gerontology - Volume 45, Issues 7â8, August 2010, Pages 512-515
نویسندگان
Ana Ugidos, Thomas Nyström, Antonio Caballero,