Past research has suggested that free radicals – occasionally harmful molecules produced by the body as it processes oxygen – contribute to the aging process. But new research from McGill University in Canada finds that free radicals may actually increase lifespan rather than shorten it.
Free radicals, also known as oxidants, are unstable and highly reactive atoms that have at least one unpaired electron. They can be formed naturally in the body or can be introduced into the body from external sources, such as smoking or pollution.
When free radicals interact with cells, proteins and DNA in the body, they can cause damage by modifying their chemical structure. Past research claims that constant cell exposure to harmful free radicals over time causes aging. But this latest study, published in the journal Cell, suggests otherwise.
The research team, including senior author Siegfried Hekimi of the Department of Biology at McGill, used a model organism – the roundworm Caenorhabditis elegans nematode – to reach their findings.
The researchers discovered that free radicals can stimulate apoptosis, also referred to as “programmed cell death” – the process by which damaged cells “commit suicide.” They may do this to avoid becoming cancerous, for example, or to destroy viruses that have taken over the cell.
The team found that when free radicals stimulate apoptosis in a certain way, the cells’ defenses are reinforced, meaning their lifespan is increased.
Explaining the team’s findings further, Hekimi says:
“People believe that free radicals are damaging and cause aging, but the so-called ‘free radical theory of aging’ is incorrect.
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.”
Hekimi adds that demonstrating the molecular mechanism by which free radicals increases the lifespan of cells provides solid evidence that they have positive effects as signaling molecules.
Furthermore, he notes that the findings mean that apoptosis signaling may be used to trigger processes that decelerate 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,” adds Hekimi. “But that doesn’t mean it will be easy.”
He says that such a process could be important in neurodegenerative diseases. He explains that apoptotic brain signaling may be focused on increasing the resistance of damaged cells rather than destroying them, since it is more difficult to replace dead neurons than other cell types as a result of the complexity in their connections.
Medical News Today recently reported on a study from the Stanford School of Medicine in California, which revealed that infusing aging mice with the blood of young mice appears to reverse age-related brain impairments.