Scientists have found an unexpected link between cell suicide and longevity, which may be the key to aging more slowly and living longer.
Researchers at McGill University's findings have showed how free radicals promote longevity in an experimental model organism, the roundworm C. elegans, and discovered that free radicals, also known as oxidants, act on a molecular mechanism that, in other circumstances, tells a cell to kill itself.
Programmed cell death, or apoptosis, is a process by which damaged cells commit suicide in a variety of situations: to avoid becoming cancerous, to avoid inducing auto-immune disease, or to kill off viruses that have invaded the cell.
The McGill researchers found that the Nobel Prize winning mechanism, which was first discovered in C. elegans, when stimulated in the right way by free radicals, actually reinforces the cell's defenses and increases its lifespan.
Professor Siegfried Hekimi, a senior author of the study said that the belief that free radicals are damaging and cause aging is incorrect, and we have turned this so-called 'free radical theory of aging' theory on its head by proving that free radical production increases during aging thus inducing a substantially longer life.
Hekimi said that the findings also mean that apoptosis signaling can be used to stimulate mechanisms that slow down aging.
The study is published in the journal Cell.
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