Oxidants combat aging to make you live longer

This may come as a real shock to you. Free radicals - also known as oxidants produced by our bodies as we process oxygen - act on a molecular mechanism that, in other circumstances, tells a cell to kill itself!

In other words, free radicals actually promote longevity, research says.

"People believe that free radicals are damaging and cause aging but the so-called 'free radical theory of aging' is incorrect," claimed Siegfried Hekimi, a professor in at Canada-based McGill University's department of biology.

"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 explained.

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 main molecular mechanism by which this happens is well conserved in all animals, but was first discovered in C. elegans - a discovery that resulted in a Nobel Prize.

The McGill researchers found that this same mechanism, when stimulated in the right way by free radicals, actually reinforces the cell's defenses and increases its lifespan.

It also means that apoptosis signaling can be used to stimulate mechanisms that slow down aging, researchers noted in a study published in the journal Cell. 

PS- THIS IS ONLY FOR INFORMATION, ALWAYS CONSULT YOU PHYSICIAN BEFORE HAVING ANY PARTICULAR FOOD/ MEDICATION/EXERCISE/OTHER REMEDIES.

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Aspirin may fight cancer by slowing DNA damage

Aspirin can lower risk for some cancers by slowing DNA 

damage, scientists have found. The study found that aspirin 

slows the accumulation of DNA mutations in abnormal cells 

in at least one pre-cancerous condition.

"Aspirin and other non-steroidal anti-inflammatory drugs, 

which are commonly available and cost-effective 

medications, may exert cancer-preventing effects by 

lowering mutation rates," said a scientist,  who analysed 

biopsy samples from 13 patients with a pre-cancerous 

condition called Barrett's oesophagus who were tracked for 

six to 19 years. DNA mutations Some patients started out 

taking daily aspirin for several years, and then stopped, 

while others started taking aspirin for the first time during 

observation. The goal was to track the rate of mutations in 

tissues sampled at different times.

The researchers found that biopsies taken while patients 

were on an aspirin  regimen had on average accumulated 

new mutations about 10 times more slowly than biopsies 

obtained during years when patients were not taking 

aspirin. Scientist now plans to test a hypothesis that may 

explain that aspirin's lowering of mutation rates is due to 

the drug's effect of reducing inflammation.

Inflammation, a response of the immune system, in recent 

years has been recognised as a hallmark of cancer. He said 

that less inflammation may result in less production within 

pre-cancerous tissue of oxidants known to damage DNA, 

and may dampen growth-stimulating signalling.

For the duration of the study, the rate of accumulation of 

mutations measured in the biopsied tissue between time 

points was slow, even when patients were not taking 

aspirin, with the exception of one patient.While mutations 

accumulated at a steady rate, the vast majority of mutations 

arose before the abnormal tissue was first detected in the 

clinic, the researchers concluded.

These findings are consistent with the fact that although 

Barrett's oesophagus is a significant risk factor for 

oesophageal cancer, the vast majority of cases do not 

progress to cancer, he said. In the one patient who later 

went on to develop cancer, a population of cellular 'clones' 

with a great number of mutations emerged shortly before he 

started taking aspirin. Rather than aiming to kill tumour 

cells, it may be better to try to halt or slow growth and 

mutation, he said. 


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