In the early 60's, Dr. Leonard Hayflick carried out research at the

Wistar Institute in Philadelphia which led to the discovery of the

"Hayflick Limit".

Hayflick found that lung tissue appeared to die out after the cells

had divided a certain number of times (roughly 50). Cell cultures

were also frozen after dividing 25 times. On revival, the cells

would continue until the 50 division limit was reached, then die.

As the cells approached the end of their division limit, the cells

would take on the appearance of old tissue. This appearance

included age pigments (lipofuscin) which is also found in aged

hearts and brain cells.

The discovery of the Hayflick Limit led to theories speculating on

the existence of a cellular "clock". These clocks could be

internally regulated for each individual cell (accounting for

variations below and above the 50 limit) or controlled systemically

by the hypothalamus of the brain.

Another possibility is that control is exerted by the DNA since DNA

is known to contain our genetic blueprints. Dr. James Fries and

Dr. Lawrence Crapo write,

"Probably, aging just happens, as the result of cumulative,

random, and inevitable errors in translation of DNA into

protein. The errors may even be a crucial part of a process

that allows variation among individuals and thus allows

natural selection."

Mistakes in cell division tend to accumulate from the actions of

viruses, free radicals, radiation and chemicals to affect the

healthy replication of DNA. As the system ages and the DNA becomes

more damaged, the DNA repair mechanism can no longer perform to its

optimum level.

Organisms and animals which have better DNA repair mechanisms tend

to live longer than those who don't.

One technique used by lower life forms is to minimize cell

replication during daylight hours to prevent radiation damage from

ionizing rays such as UV.