Suggesting that Mitochondrial DNA Damage Doesn't Result From Oxidative Stress
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Mitochondria are the power plants of the cell: they produce chemical energy stores and participate in an important way in numerous other vital cellular processes. Mitochondria contain their own DNA, left over from their past existence as symbiotic bacteria, and damage to this mitochondrial DNA is a contributing cause of aging. The conventional view is that this damage arises when the reactive oxygen species produced by mitochondria in the course of their normal operation react with the nearby DNA. This is supported by a wide range of evidence, such as the fact that antioxidants targeted to mitochondria extend life.

These researchers offer evidence in support of another view - that oxidative stress doesn't matter, and the damage that contributes to aging occurs during mitochondrial replication. This view leaves numerous open questions, such as what is happening to extend life via targeted antioxidants:

Mitochondria are the evolutionary remnants of bacteria that were acquired by the cells of our ancestors more than a billion years ago and now produce virtually all of the cellular energy. Due to their bacterial ancestry, mitochondria have their own genomes, which encode some of the machinery responsible for producing energy. These genes occasionally acquire mutations - irreversible alterations that can adversely affect the energy production machinery. The accumulation of mitochondrial DNA (mtDNA) mutations is thought to cause aging and common age-related diseases, but we know little about the factors that influence the frequency of these mutations.

Our study tested whether fruit flies would serve as a good animal model to study this problem. We found that flies accumulate mtDNA mutations in a pattern similar to that of humans. We then used flies to test the long-standing theory that toxic free radicals, chemical byproducts of energy production, cause mtDNA mutations to accumulate. Our data do not support this hypothesis, and instead suggest that rare errors associated with duplicating mitochondrial genomes are primarily responsible for mtDNA mutations. In sum we demonstrate that Drosophila serves as a tractable genetic model to investigate the mechanisms that influence the frequency of somatic mtDNA mutations.


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