Unanticipated Link Found Between Cell Suicide and Long Life

Many health professionals believe that free radicals, the occasionally toxic molecules generated by the body as it processes oxygen, are the cause behind aging. However, a number of studies recently have generated evidence that the contrary may be true.

Researchers from McGill University (Montreal, QC, Canada) have taken this finding further by showing how free radicals promote longevity in a research model organism, the roundworm Caenorhabditis elegans. Unexpectedly, the scientists discovered that free radicals (i.e., oxidants) act on a molecular mechanism that, in other surroundings, instructs a cell to kill itself.


Apoptosis is a process by which injured cells commit suicide in a range of circumstances: to avoid inducing autoimmune disease, to avoid becoming cancerous, or to kill off viruses that have invaded the cell. The key molecular mechanism by which this occurs is well conserved in all animals, but was first discovered in C. elegans—a finding that earned a Nobel Prize.

The McGill University researchers discovered that this same mechanism, when stimulated in the correct manner by free radicals, in reality strengthens the cell’s defenses and increases its longevity. Their findings were published online May 8, 2014, in the journal Cell. “People believe that free radicals are damaging and cause aging, but the so-called ‘free radical theory of aging’ is incorrect,” said Siegfried Hekimi, a professor in McGill’s department of biology, and senior author of the study. “We have turned this theory on its head by proving that free radical production increases during aging because free radicals actually combat—not cause—aging. In fact, in our model organism we can elevate free radical generation and thus induce a substantially longer life.”

The findings have significant ramifications. “Showing the actual molecular mechanisms by which free radicals can have a pro-longevity effect provides strong new evidence of their beneficial effects as signaling molecules,” Prof. Hekimi said. “It also means that apoptosis signaling can be used to stimulate mechanisms that slow down aging. Since the mechanism of apoptosis has been extensively studied in people, because of its medical importance in immunity and in cancer, a lot of pharmacological tools already exist to manipulate apoptotic signaling. But that doesn’t mean it will be easy.”

Triggering pro-longevity apoptotic signaling could be especially critical in neurodegenerative disorders, according to Prof. Hekimi. “In the brain the apoptotic signaling might be particularly tilted toward increasing the stress resistance of damaged cells rather than killing them. That’s because it is harder to replace dead neurons than other kinds of cells, partly because of the complexity of the connections between neurons.”

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