Ongoing Careful Analysis of Mitochondria and Longevity

Mitochondria are the power plants of the cell, the evolved remnants of what were originally symbiotic bacteria, and which still possess their own fragile DNA distinct from that in the cell nucleus. They churn away producing the adenosine_triphosphate (ATP) used as an energy source in cellular processes, and are clearly of great importance in determining longevity. Scientists have for some years been carefully pulling apart the core mitochondrial machinery to better understand why this is the case, and here is an example of this ongoing research: "A decrease in mitochondrial electron transport chain (ETC) activity results in an extended lifespan in Caenorhabditis elegans. This longevity has only been reported when complexes I, III and IV genes are silenced, but not genes of complex II. We now have suppressed each complex II subunit in turn and have confirmed that in no case is lifespan extended. Animals with impaired complex II function exhibit similar metabolic changes to those observed following suppression of complexes I, III and IV genes, but the magnitude of the changes is smaller. Furthermore, an inverse correlation exists between mitochondrial membrane potential and ATP levels, which strongly suggests that dynamic allocation of energy resources is maintained. In contrast, suppression of genes from complexes I, III and IV, results in a metabolic crisis with an associated stress response and loss of metabolic flexibility. Thus, the maintenance of a normal metabolism at a moderately decreased level does not alter normal lifespan, whereas metabolic crisis and induction of a stress response is linked to lifespan extension."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22122855

Comments

I think mito function is the biggest contributor to aging, and I have done a lot of reading on the subject. But I must admit some of this discussion is over my head. Nonetheless, I think the last line is quite noteworthy. "...the maintenance of a normal metabolism at a moderately decreased level does not alter normal lifespan, whereas metabolic crisis and induction of a stress response is linked to lifespan extension"

Maybe I am misinterpreting this, but it seems to be consistent with my philosopy of intermittent (weekly) fasting in order to induce autophagy (stress responose) in the mito.

Posted by: JohnD at December 1st, 2011 7:40 AM

Here are a couple of recent encouraging articles from The Journal of Neuroscience on the efficacy of MitoQ (the mitochodia-targetted antioxidant):

"The Mitochondria-Targeted Antioxidant MitoQ Prevents Loss of Spatial Memory Retention and Early Neuropathology in a Transgenic Mouse Model of Alzheimer's Disease"
http://www.jneurosci.org/content/31/44/15703.short

"Mitochondrial Dysfunction in SOD1G93A-Bearing Astrocytes Promotes Motor Neuron Degeneration: Prevention by Mitochondrial-Targeted Antioxidants"
http://www.jneurosci.org/content/28/16/4115.abstract

Posted by: Lou Pagnucco at December 1st, 2011 10:46 AM

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