Drinking gallons of orange juice and popping vitamin pills may not make you live longer, say US researchers, contrary to previous reports
In the past, scientists have suggested that taking antioxidants to combat free radical cell damage might delay ageing.
But a University of Wisconsin-Madison team has found no proof that highly reactive oxygen molecules are involved.
Instead, cells committing early suicide is key – at least in rodents – they told the journal Science.
Rapid ageing
However, both ageing theories do involve damage to the cell’s genetic material – DNA.
The mice the US researchers looked at were engineered to age prematurely. This was because they lacked a protein that effectively proof reads DNA for mistakes.
As a consequence, the altered mice had far more DNA errors within the power houses of cells – structures called mitochondria.
In turn, this prompted cells to die off.
Compared with normal mice, the altered mice also developed obvious signs of ageing, such as grey hair and muscle wasting, at a much quicker rate.
"We think that the key to what is happening in ageing is that as mutations or DNA damage accumulates, critical cells die," said Dr Prolla.
Cell death
These critical cells might include adult stem cells that are essential for replacing the cells that die, he said.
"If these stem cells are lost, tissue structure and the ability of tissue to regenerate are impaired.
"We have observed that in tissues like bone marrow, intestine and hair follicles," said Dr Prolla.
Dr Aubrey de Grey, an expert in ageing research at the University of Cambridge, said: "This is an important study, building on similar work by a couple of other groups over the past few years.
"It would be premature to say that these studies are conclusive with regard to the role of mitochondrial mutations in ageing, but they certainly imply that cell death, especially of stem cells, can make a big difference to the rate of ageing."
He said it was important to be cautious because it was impossible to be sure that something which shortens life if you accelerate it is also lifespan-limiting when it proceeds at its natural rate.
"Ideally, we would develop mice that had better mitochondrial DNA repair and maintenance and lived longer as a result, but we don’t have that result yet."