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Exp Gerontol. 2010 Aug;45(7-8):512-5. doi: 10.1016/j.exger.2010.02.002. Epub 2010 Feb 12.

Perspectives on the mitochondrial etiology of replicative aging in yeast.

Author information

1
Department of Cell and Molecular Biology, Göteborg University, Medicinaregatan 9C, Göteborg, Sweden.

Abstract

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.

PMID:
20153818
DOI:
10.1016/j.exger.2010.02.002
[Indexed for MEDLINE]

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