File this one under “I didn’t see it coming”: Mitochondria can be introduced into cells by simply co-incubating the two, allowing cells with damaged or dysfunctional mitochondria to recover efficient respiration. Since mitochondria accumulate damage with aging, the ability to transfer new mitochondria into aged cells could reverse age-relate decline in energy production, and lift cells out of the vicious cycle whereby oxidative radicals cause mitochondrial damage, which in turn increases the rate of oxidative radical production. From Katrangi et al.:

Xenogenic Transfer of Isolated Murine Mitochondria into Human ρ0 Cells Can Improve Respiratory Function

Mitochondrial DNA mutations are the direct cause of several physiological disorders and are also associated with the aging process. The modest progress made over the past two decades towards manipulating the mitochondrial genome and understanding its function within living mammalian cells means that cures for mitochondrial DNA mutations are still elusive. Here, we report that transformed mammalian cells internalize exogenous isolated mitochondria upon simple co-incubation. We first demonstrate the physical presence of internalized mitochondria within recipient cells using fluorescence microscopy. Second, we show that xenogenic transfer of murine mitochondria into human cells lacking functional mitochondria can functionally restore respiration in cells lacking mtDNA. Third, utilizing the natural competence of isolated mitochondria to take up linear DNA molecules, we demonstrate the feasibility of using cellular internalization of isolated exogenous mitochondria as a potential tool for studying mitochondrial genetics in living mammalian cells.

This is a far cry from introducing mitochondria into intact tissues, but many types of cells can be removed from the body and then re-introduced, so a similar strategy could be employed for bone-marrow or other stem cell populations. Presumably, cells with fresh mitochondria would be more capable of re-growth after re-introduction, possibly pushing out unrepaired cells by outcompeting them for space in stem cell niches.

I’d certainly like to see this repeated in non-transformed cells — transformed cells do all kinds of weird things, after all, and that may well include hyperactive glorping of nearby small particles. The ρ0 experiment goes a fair way toward allaying my skepticism on that subject — cells lacking mitochondria are notoriously sluggish, and if both transformed and ρ0 cells can do something I’m more inclined to believe that all cells can do it — still, if we are to believe that this is a general feature of all cells, I’d like to see a clear demonstration that normal somatic and stem cells are capable of this neat trick.

Note also that the authors introduced murine mitochondria into human cells, apparently without incompatibility; they point out that mitochondria are naturally competent to take up exogenous DNA — i.e., they can be readily engineered. Could we create hybrid human cells with the mitochondria of whales? The anti-doping agencies of the future may have to watch out for souped-up runners with greyhound mitochondria in their muscles…

(Hat tip to Fight Aging!)