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Journal ArticleDOI

The Mitochondrial Theory of Aging

Axel Kowald
- 24 May 2001 - 
- Vol. 10, pp 162-175
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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.

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Melatonin as an antioxidant: under promises but over delivers.

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Mitochondria as a Target of Environmental Toxicants

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Ryanodine Receptor Oxidation Causes Intracellular Calcium Leak and Muscle Weakness in Aging

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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

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

TL;DR: This finding demonstrated that a nucleotide change in a mitochondrial DNA energy production gene can result in a neurological disease.
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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.
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