Journal ArticleDOI
The Mitochondrial Theory of Aging
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TLDR
The idea that genetically damaged mitochondria accumulate with time and are causally responsible for the aging phenotype via a disturbed energy budget is at the core of the so called mitochondrial theory of aging.Abstract:
Mitochondria are not only the main source of energy for most eukaryotic cells, but also the main source of free radicals. These reactive molecules can damage all components of a cell such as membranes, proteins and DNA. Therefore they have long been suspected to be involved in the biological aging process. The fact that mitochondria posses their own genetic material (mtDNA) and that they only have a limited arsenal of DNA repair processes makes them one of the prime targets for reactive oxygen species. The idea that genetically damaged mitochondria accumulate with time and are causally responsible for the aging phenotype via a disturbed energy budget is at the core of the so called mitochondrial theory of aging. In recent years this idea has gained impetus from the discovery of mitochondrial diseases and mtDNA deletions in old organisms. However, there are still many open questions regarding the mechanism of the accumulation of these deletions and their physiological relevance. This review is therefore intended to give an overview of the current state of the mitochondrial theory of aging and to discuss some recent experimental findings.read more
Citations
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Journal ArticleDOI
Research Agenda for Frailty in Older Adults: Toward a Better Understanding of Physiology and Etiology: Summary from the American Geriatrics Society/National Institute on Aging Research Conference on Frailty in Older Adults
Jeremy D. Walston,Evan C. Hadley,L. Ferrucci,Jack M. Guralnik,Anne B. Newman,Stephanie A. Studenski,William B. Ershler,Tamara J. Harris,Linda Fried +8 more
TL;DR: The results of the 2004 American Geriatrics Society/National Institute on Aging conference on a Research Agenda on Frailty in Older Adults, which brought together a diverse group of clinical and basic scientists to encourage further investigation in this area are reported on.
Journal ArticleDOI
Melatonin as an antioxidant: under promises but over delivers.
Russel J. Reiter,Juan C. Mayo,Dun Xian Tan,Rosa M. Sainz,Moisés Alejandro Alatorre-Jiménez,Lilian Qin +5 more
TL;DR: It is the current feeling of the authors that, in view of the widely diverse beneficial functions that have been reported for melatonin, these may be merely epiphenomena of the more fundamental, yet‐to‐be identified basic action(s) of this ancient molecule.
Journal ArticleDOI
Mitochondria as a Target of Environmental Toxicants
Joel N. Meyer,Maxwell C.K. Leung,John P. Rooney,Ataman Sendoel,Michael O. Hengartner,Glen E. Kisby,Amanda S. Bess +6 more
TL;DR: The fields of environmental toxicology and environmental health should focus more strongly on mitochondria, with a particular focus on those toxicants that target mitochondrial DNA.
Journal ArticleDOI
Pathological aspects of lipid peroxidation
Anne Nègre-Salvayre,Nathalie Augé,Victoria Ayala,Huveyda Basaga,Jordi Boada,Rainer Brenke,Sarah J. Chapple,Guy Cohen,János Fehér,Tilman Grune,Gabriella Lengyel,Giovanni E. Mann,Reinald Pamplona,Giuseppe Poli,Manuel Portero-Otin,Yael Riahi,Robert Salvayre,Shlomo Sasson,José C. E. Serrano,Ofer Shamni,Werner Siems,Richard C.M. Siow,Ingrid Wiswedel,Kamelija Zarkovic,Neven Zarkovic +24 more
TL;DR: Striking evidences implicating LPO in foetal vascular dysfunction occurring in pre-eclampsia, in renal and liver diseases, as well as their role as cause and consequence to cancer development are addressed.
Journal ArticleDOI
Ryanodine Receptor Oxidation Causes Intracellular Calcium Leak and Muscle Weakness in Aging
Daniel C. Andersson,Matthew J. Betzenhauser,Steven Reiken,Albano C. Meli,Alisa Umanskaya,Wenjun Xie,Takayuki Shiomi,Ran Zalk,Alain Lacampagne,Andrew R. Marks +9 more
TL;DR: Treating aged mice with S107 stabilized binding of calstabin1 to RyR1, reduced intracellular calcium leak, decreased reactive oxygen species (ROS), and enhanced tetanic Ca(2+) release, muscle-specific force, and exercise capacity indicate that leaky RyR 1 contributes to age-related loss of muscle function.
References
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Book
Free radicals in biology and medicine
TL;DR: 1. Oxygen is a toxic gas - an introduction to oxygen toxicity and reactive species, and the chemistry of free radicals and related 'reactive species'
Journal ArticleDOI
Sequence and organization of the human mitochondrial genome
Stephen Anderson,Alan T. Bankier,Bart Barrell,M.H.L. de Bruijn,Alan Coulson,J. Drouin,J. Drouin,Ian C. Eperon,Donald P. Nierlich,Donald P. Nierlich,Bruce A. Roe,Bruce A. Roe,Frederick Sanger,P. H. Schreier,Andrew J.H. Smith,Rodger Staden,Ian G. Young,Ian G. Young +17 more
TL;DR: The complete sequence of the 16,569-base pair human mitochondrial genome is presented and shows extreme economy in that the genes have none or only a few noncoding bases between them, and in many cases the termination codons are not coded in the DNA but are created post-transcriptionally by polyadenylation of the mRNAs.
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Mitochondrial DNA mutation associated with Leber's hereditary optic neuropathy
Douglas C. Wallace,Gurparkash Singh,Marie T. Lott,Judy A. Hodge,Theodore G. Schurr,Angela M. S. Lezza,Louis J. Elsas,Eeva K. Nikoskelainen +7 more
TL;DR: This finding demonstrated that a nucleotide change in a mitochondrial DNA energy production gene can result in a neurological disease.
Journal ArticleDOI
A mutation in the tRNA Leu(UUR) gene associated with the MELAS subgroup of mitochondrial encephalomyopathies
TL;DR: An A-to-G transition mutation at nucleotide pair 3,243 in the dihydrouridine loop of mitochondrial tRNALeu(UUR) that is specific to patients with MELAS is reported, which creates an Apal restriction site and could perform a simple molecular diagnostic test for the disease.
Journal ArticleDOI
The Biologic Clock: The Mitochondria?
TL;DR: The author suggests that the maximal life span of a given mammalian species is largely an expression of genetic control over the rate of oxygen utilization, the rate increasing with the rates of oxygen consumption, which ultimately causes death.