Of Mice and Mitochondria
I was going to post some thoughts on the recently reported hard proof for mitochondrial theories of aging, but Randall Parker has already done an excellent job of that at FuturePundit. I quote a fair amount below, but you should read the whole thing:
Mice genetically engineered to have a defective mechanism for repairing only the DNA found in mitochondria age more rapidly and have less than half the life expectancy of normal mice....
Mitochondria are organelles that exist inside all eukaryotic cells (most complex life forms including humans have eukaryotic cells) and function to break down sugars to produce energy. Mitochonida have their own DNA for a small subset of their proteins. The Swedish team introduced a mutation to break a repair mechanism for the DNA in mitochondria in order to study how important accumulation of damage to mitochondrial DNA is to the overall rate of aging. The results suggest that damage accumulation to mitochondrial DNA is as important as some scientists have argued for years.
...
Why does the accumulation of mitochondrial DNA damage accelerate aging? One obvious possibility is that the DNA damage knocks out genes needed for energy production and hence cells begin to malfunction due to a lack of energy. But another quite plausible possibility is that the mutations knock out steps in sugar metabolism in a way that leads to the generation of lots of free radicals. In this model (suggested by Aubrey de Grey - more about him below) the cells that have defective mitochondria become toxic free radical generators for all the cells around them. In essence, a fairly small number of cells become mini-toxic waste sites. Someone call in the Environmental Protection Agency. This sort of thing should be forbidden by tough pollution law enforcement.
He goes on to discuss Aubrey de Grey's proposals to alter cells to make mitochondrial damage less unhealthy:
Aubrey has repeatedly argued for funding of experimental work to move genes into the nucleus of a mouse cell to then be used to clone and raise mice that have all their mitochondrial genes in their nuclei. The effect might be the opposite of the experiment reported above. Rather than shortening life the mice might live much longer. Such a result would lend further support for the argument that mitochondrial DNA gene therapy should be developed as a rejuvenation technique.
I imagine that this would a logical next step for researchers to look into. I also imagine that Aubrey de Grey is spending a lot of time on the phone right now...