Antioxidant possible feedbacks

[whoa182]

This was just posted today from Kevin Perrott on the mprize.org website and Health Extension

 

Rafal Smigrodzki and Mitochondrial Gene Therapy

 

Mitochondrial DNA has long been the number one suspect in aging since Denham Harman first proposed the Mitochondrial Theory of Aging in 1972. It has taken some years however to accumulate enough evidence in order to categorically state that the theory is more than just a theory. Recent studies which demonstrated life span extension in a mitochondrial catalase expressing transgenic mouse have quite effectively shown that mitochondria indeed play a large part in the aging process.

 

Recently Rafal brought his ideas to the fore and I obtained a pre-publication copy of his paper regarding the Theory of Microheteroplasmy and its role in the aging process. Basically the theory states that as our methods for detecting mtDNA mutations have become more sensitive, it has become apparent that more than 90% of our mtDNA is mutated by adult life. He proposes that the mutation burden of mitochondria, although specific species may comprise less than 3% each, together combine to cause age related disease and point an even sharper finger at mitochondrial degneration as the main culprit in the aging process.

 

A second and perhaps more controversial part of Rafal's talk dealt with his as yet unverified method of "protofection" where mutant mitochondrial DNA is replaced using genetic techniques which transport the DNA into the mitochondria itself. Thus far and because the paper is not yet accepted for publication, Rafal has been unable to provide the protocols so the methods can be verified independently. He did however provide some nice slides and pictures of gels which would indicate that the procedure and phenomenon is reproducible. I for one will be very anxious to test Rafal's proposed methods on my C. elegans subjects!

 

If wholesale mitochondrial gene therapy becomes available AND microheteroplasmy indeed turns out to be critical to the aging process, it is possible that this may be one of the most significant discoveries yet in biogerontology. Of course there is much remaining to prove regarding Smigrodzki's theories but we are fortunate to be in a time when the analysis of mtDNA can be accomplished at such a fine level that mutations present at less than 3% can be determined at all.

 

Download the Real Media presentation (61MB) Here (click the right mouse button and choose Save As...).

[UncleAl]

No.

[Biochemist]

UncleAl gets the "concise" award.

 

Most cells reach death after a predetermjined number of generations. It would be possible (probably soon) to recreate a clone of an adult from the adult's germ cells, but that would not extend the adult life. We would just have a younger twin. We will not likely reverse or forestall cell death in each of your several trillion cells with either genetic engineering or antioxidants. Antioxidants are pretty blunt instruments that mitigate the damage casued by a small number of toxic chemicals. Genetic therapies may well have some success in mitigating specific genetic failings (like replacing dysfunctional islet cells in the pancreas) but the notion of replenishing millions of different highly differentiated cells types in adults is untenable. Further, the delivery systems (to get the genetic material to the target bioshpere) is a problem in themselves.

 

Essentially, UncleAl is correct.