DNA, Mitochondrial

Publication Title: 
Mutation Research

During the course of normal respiration, reactive oxygen species are produced which are particularly detrimental to mitochondrial function. This is shown by recent studies with a mouse that lacks the mitochondrial form of superoxide dismutase (Sod2). Tissues that are heavily dependent on mitochondrial function such as the brain and heart are most severely affected in the Sod2 mutant mouse.

Author(s): 
Melov, S.
Coskun, P. E.
Wallace, D. C.
Publication Title: 
Best Practice & Research. Clinical Endocrinology & Metabolism

Sex differences in lifespan exist world-wide, with women outliving men by more than a decade in some countries. The gender gap is not a uniquely human phenomenon; most sexually reproducing species examined show sex differences in patterns of ageing, yet a comprehensive explanation does not exist. Here, we discuss how ageing responds to natural selection on traits that arise as a consequence of sexuality.

Author(s): 
Regan, Jennifer C.
Partridge, Linda
Publication Title: 
PloS One

BACKGROUND: Longevity is a multifactorial trait with a genetic contribution, and mitochondrial DNA (mtDNA) polymorphisms were found to be involved in the phenomenon of longevity. METHODOLOGY/PRINCIPAL FINDINGS: To explore the effects of mtDNA haplogroups on the prevalence of extreme longevity (EL), a population based case-control study was conducted in Rugao--a prefecture city in Jiangsu, China. Case subjects include 463 individuals aged > or = 95 yr (EL group).

Author(s): 
Cai, Xiao-yun
Wang, Xiao-Feng
Li, Shi-lin
Qian, Ji
Qian, De-gui
Chen, Fei
Yang, Ya-Jun
Yuan, Zi-yu
Xu, Jun
Bai, Yidong
Yu, Shun-Zhang
Jin, Li
Publication Title: 
Advances in Experimental Medicine and Biology

Aging is a degenerative process that is associated with progressive accumulation of deleterious changes with time, reduction of physiological function and increase in the chance of disease and death.

Author(s): 
Lee, Hsin-Chen
Wei, Yau-Huei
Publication Title: 
Age (Dordrecht, Netherlands)

Mitochondria produce cellular energy but also free-radicals, which damage cells despite an array of endogenous anti-oxidants. In Northern Europe, the mitochondrial haplogroup J has been related to longevity in nonagenarians and centenarians but also with age-related disease. Hypertension is an important contributor to atherosclerotic-related diseases and its pathogenesis is associated with increased oxidative stress.

Author(s): 
Rea, Irene Maeve
McNerlan, Susan E.
Archbold, G. Pooler
Middleton, Derek
Curran, Martin D.
Young, Ian S.
Ross, Owen A.
Publication Title: 
BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology

Mitochondrial function is achieved through the cooperative interaction of two genomes: one nuclear (nuDNA) and the other mitochondrial (mtDNA). The unusual transmission of mtDNA, predominantly maternal without recombination is predicted to affect the fitness of male offspring. Recent research suggests the strong sexual dimorphism in aging is one such fitness consequence. The uniparental inheritance of mtDNA results in a selection asymmetry; mutations that affect only males will not respond to natural selection, imposing a male-specific mitochondrial mutation load.

Author(s): 
Wolff, Jonci N.
Gemmell, Neil J.
Publication Title: 
Cellular and molecular life sciences: CMLS

Reduction of nutrient intake without malnutrition positively influences lifespan and healthspan from yeast to mice and exerts some beneficial effects also in humans. The AMPK-FoxO axis is one of the evolutionarily conserved nutrient-sensing pathways, and the FOXO3A locus is associated with human longevity. Interestingly, FoxO3A has been reported to be also a mitochondrial protein in mammalian cells and tissues. Here we report that glucose restriction triggers FoxO3A accumulation into mitochondria of fibroblasts and skeletal myotubes in an AMPK-dependent manner.

Author(s): 
Peserico, Alessia
Chiacchiera, Fulvio
Grossi, Valentina
Matrone, Antonio
Latorre, Dominga
Simonatto, Marta
Fusella, Aurora
Ryall, James G.
Finley, Lydia W. S.
Haigis, Marcia C.
Villani, Gaetano
Puri, Pier Lorenzo
Sartorelli, Vittorio
Simone, Cristiano
Publication Title: 
Biochemical Society Transactions

Although there is general agreement that most forms of common disease develop as a consequence of a combination of factors, including genetic, environmental and behavioural contributors, the actual mechanistic basis of how these factors initiate or promote diabetes, cancer, neurodegenerative and cardiovascular diseases in some individuals but not in others with seemingly identical risk factor profiles, is not clearly understood.

Author(s): 
Ballinger, Scott W.
Publication Title: 
Annual Review of Physiology

Genome instability has long been implicated as the main causal factor in aging. Somatic cells are continuously exposed to various sources of DNA damage, from reactive oxygen species to UV radiation to environmental mutagens. To cope with the tens of thousands of chemical lesions introduced into the genome of a typical cell each day, a complex network of genome maintenance systems acts to remove damage and restore the correct base pair sequence.

Author(s): 
Vijg, Jan
Suh, Yousin
Publication Title: 
Gerontology

A fundamental impact of mitochondria on biological aging has been suggested decades ago. One prominent theory explains aging as the result of the age-related accumulation of random molecular damage of biomolecules resulting from the reaction of reactive oxygen species, the majority of which are generated in mitochondria. Although this concept appeared to be very attractive and strongly influenced aging research, in recent years more and more data accumulated which seem to contradict this theory.

Author(s): 
Osiewacz, Heinz D.
Bernhardt, Dominik

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