An anti-ageing pill that delays the onset of wrinkles and crow's feet could be on the horizon, scientists believe.

Telomeres - protective bits of DNA on the end of chromosomes - become shorter every time a cell divides, new research found.

Experts say this causes people to age and increases their risk of disease as they grow older.

But a study found levels of the enzyme telomerase - which lengthens the protective tips - are higher in cancer cells.

This allows them to divide indefinitely - offering scientists hope of developing drugs that could target the mechanism to prevent ageing.

An anti-ageing pill that delays the onset of wrinkles and crows feet could be on the horizon, scientists believe

Experts also believe their findings could provide benefits in the bid to find a cure for cancer.

When telomeres become too short they send a signal to the cell to stop dividing permanently – impairing the ability of tissues to regenerate.

They play key roles in inflammation and contribute to many ageing-related diseases – including cancer.

Previous research has found oxidative stress – where damaging molecules known as free radicals build up inside cells – speeds up the process.

Free radicals can damage both the DNA that make up telomeres but also the building blocks used to extend them.

Researchers from Pittsburgh University tested to see if oxidative stress would render telomerase unable to do its job.

They then looked to see what would happen if the building blocks used to make up telomeres were instead subjected to the damage.

Their findings suggest telomere is shortened by free radicals damaging the building block molecules - not the enzyme itself.

Telomeres - protective bits of DNA on the end of chromosomes - become shorter every time a cell divides. This allows them to divide indefinitely and causes people to age - offering scientists hope of developing drugs that could target the mechanism

Lead researcher Professor Patricia Opresko, of Pittsburgh University, said: 'The new information will be useful in designing new therapies to preserve telomeres in healthy cells and ultimately help combat the effects of inflammation and ageing.

'On the flip side we hope to develop mechanisms to selectively deplete telomeres in cancer cells to stop them from dividing.

'Much to our surprise telomerase could lengthen telomeres with oxidative damage. In fact the damage seems to promote telomere lengthening.'

Nell Barrie, Cancer Research UK's senior science information manager, said: 'Telomeres can act like a "clock" inside cells telling them when it's the right time to self-destruct.

'But this process can be disrupted in cancer and other diseases so understanding exactly what is happening inside cells will give researchers clues for how to correct mistakes and take advantage of cells' strengths and weaknesses to help treat disease.

'There's still a lot we need to understand about how the telomeres "clock" works and research like this will help to shed light on its inner workings.'