A Little Mitochondrial Science

A little mitochondrial science for you today, culled from the interesting material posted to sci.life-extension. A great deal of investigation is taking place into damage and decline of mitochondria, and how it relates to age-related degeneration, frailty and illness. The more that researchers understand of the biochemistry at the root of this process, the sooner medical science will deliver therapies to put a stop to this aspect of aging. It's just like fixing up a car: if you know how to do it, you can do it, and your car lasts longer as a result.

Direct repeats in mitochondrial DNA and mammalian lifespan:

Mitochondria have long been suspected to be among the leading determinants of aging due to their functional importance and accelerated deterioration caused by accumulation of mutations in the [mitochondrial DNA (mtDNA). Direct repeats are known to contribute to deletion formation in mtDNA and are a powerful source of reactive oxygen species (ROS)-independent mutagenesis. To evaluate the potential importance of homology-based deletion formation, we have analyzed the association between direct repeats in the mtDNA sequence and the lifespans of 65 mammalian species. Here, we report a significant negative correlation between the mutagenic potential of direct repeats and the mammalian lifespan, which is especially evident in closely related species.

Evidence for Selective Mitochondrial Autophagy and Failure in Aging:

Autophagy is a major intracellular degradation/recycling system ubiquitous in eukaryotic cells. It contributes to the turnover of cellular components by delivering portions of the cytoplasm and organelles to lysosomes, where they are digested.


autophagy plays an important role in the degradation of excess or injured organelles, including mitochondria. To test the hypothesis of an involvement of a decrease in autophagy in the process of aging, we explored the antiaging effects of pharmacological stimulation of autophagy on the age-dependent accumulation of 8-OHdG-rich mitochondria in rat liver.


Results showed that drug injection rescued older cells from the accumulation of 8-OHdG in the mtDNA in less than 6 hours, but no significant decrease in the level of cytocrome c oxidase activity was observed. Together, these data provide indirect evidence that 8-OHdG might accumulate in a small pool of mitochondria with increasing age rather than be degraded by the autophagic machinery selectively.

These are confirming studies, elaborating and investigating the details of what is already generally known. Of such modest steps is progress built.

Meanwhile, the Methusalah Foundation has commenced research into SENS technologies that might offer a direct path towards preventing damage to mitochondria.

Mutations to the mtDNA inevitably accumulate leading to dysfunction of mitochondria, and contributing to aging of the organism. The goal of MitoSENS is to obviate mtDNA mutations by expressing the mtDNA genes from the nucleus.

Fortunately, we would be completing a process that evolution has already started.

The mitochondrial genome originally had thousands of genes, but evolution has reduced it to a mere 13 (protein encoding) genes in humans. By studying how nature transfered expression of other genes from the mitochondria to the nucleus, we can identify the necessary steps to transfer the remaining 13 genes (in humans).

This is a small amount of funding and research time at first, made possible by generous donations to the Foundation, but these efforts will expand. They join other more direct research initiatives, such as the wholesale replacement of damaged mitochondrial DNA via protofection. One of the central points of SENS is that while our knowledge is far from perfect, we know enough to get started on the development of effective, scientific anti-aging technologies today.

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