The assumption that free radicals are to blame for the aging of organisms is still widespread, although, in recent years, studies have indicated that the opposite is true. In an animal model, Canadian researchers have now succeeded in proving that oxidants may even prolong life. The study was published in "Cell".

For their study, researchers from McGill University in Montreal used the roundworm Caenorhabditis elegans. The process of apoptosis, the controlled suicide of damaged cells or cells invaded by viruses, was first discovered in this organism, which resulted in a Nobel Prize in 2002. Using this model organism, the Canadian researchers were able to show that free radicals affect a molecular process that, under certain circumstances, triggered apoptosis. In addition, the researchers discovered that the same molecular process, if it was initiated in the right way by oxidants, strengthened cell defence and prolonged its lifespan.

"People believe that free radicals are damaging and cause aging, but the so-called 'free radical theory of aging' is incorrect", says senior author Siegfried Hekimi. "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 our model organism we can elevate free radical generation and thus induce a substantially longer life."

Therefore, the researchers see far-reaching implications: "That free radicals can have a pro-longevity effect provides strong new evidence of their beneficial effects as signalling molecules. It also means that apoptosis signalling can be used to stimulate mechanisms that slow down aging", says Hakimi. "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 signalling. But that doesn't mean it will be easy."