The latest issue of Rejuvenation Research is available online. Attila Csordás of Pimm - who happens to be a molecular biologist in addition to a pro-life-extension blogger - is published therein; folks who recently picked up on the (probably quite important) factoid that our cells may transfer mitochondria or mitochondrial DNA back and forth will find his commentary interesting:

Experiments recently reported by the Prockop laboratory show that some form of mitochondrial transfer can occur among cells in vitro and can have a physiologic role by rescuing the respiration of respiration-deficient cells. However, these results do not establish whether it was only [mitochondrial DNA] or whole functional mitochondria that were transferred, or if the latter, whether the mitochondria were transferred through direct cytoplasmic transport or as discrete vesicles. Two hypotheses are discussed here concerning the physiologic role of mitotransfer (the first is preferred): (a) respiration-competent mitochondria transfer from respiration-competent cells to respiration-deficient cells with damaged mitochondria (the "entropy" scenario); and (b) respiration-competent mitochondria transfer from predominantly respiration-deficient cells to respiration-competent cells, which provide a more favorable host environment (the "selfish" scenario).

As you all no doubt know, molecular damage to the functionality of mitochondria features prominently in the mitochondrial free radical theory of aging - it's the starting point of a cascade of events that wind up causing a fraction of age-related damage, disease and frailty.

The theory as it stands rather assumes that mitochondria and their fragile DNA do not shuttle around from cell to cell in any significant numbers, however; this new research provides an interesting twist that people will no doubt be exploring and integrating in years ahead. From a practical standpoint, might this explain the rapid success of scientists who introduced fresh, undamaged mitochondrial DNA into mice via the protofection technique? Or perhaps it is a separate mechanism that could be utilitized in the same way - to mass-replace damaged mitochondria and therefore remove their contribution to the aging process.

What interesting times we live in, that we are so tantalizingly close to repairing the accumulating root cause of an entire class of age-related disease and cellular damage.

Technorati tags: biotechnology, life extension, SENS

Posted by Reason at November 18, 2006 4:44 PM | TrackBack (0)