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Cellular senescence is a process associated with aging and longevity determination
that occurs at the level of our cells. Cellular senescence is sometimes
called replicative senescence. Forty years ago, Dr. Leonard Hayflick and
his colleague, Dr. Paul Moorhead, discovered that many human cells--particularly
fibroblast cells, which secrete substances that provide structure to tissues--had
a limited capacity to reproduce themselves in culture by dividing. They
found that these and many other normal human cells derived from fetal, embryonic
or newborn tissue can undergo between 40 and 60 cell divisions, but then
can divide no more. This number is often referred to as the Hayflick Limit.
Hayflick also pointed out in a second report that there are two classes
of cells: normal mortal cells and immortal cancer cells.
Some scientists today believe that what determines the Hayflick Limit
for dividing cells is the length of cells' telomeres (see the Telomeres
Information Center). Telomeres can be pictured as caps on the ends
of chromosomes. Each time a cell divides, it must first double its chromosomes,
so that each daughter cell receives a full complement of genetic material.
But each time a chromosome reproduces itself, it loses a small bit of
its telomeres. When a cell's telomeres have reached a critically short
length, after 40 to 60 population doublings in young human cells, the
cell can no longer replicate its chromosomes and thus will stop dividing.
These cells with shortened telomeres that can no longer divide become
what is called "senescent." Cells taken from older humans divide
fewer times before this occurs. In other animals, the number of population
doublings their cultured normal cells can undergo differs from that of
humans. This number generally correlates with the length of the species'
life span.
Scientists have also noted that senescent cells are different from their
younger counterparts. Like older people entering retirement, cells approaching
senescence incur many biological losses or take on new functions. Where
younger cells might produce structural or functional proteins, cells approaching
senescence might release enzymes that break down these proteins.
Senescent cells are not only associated with certain age-related diseases,
but may also be a direct reflection of the aging and longevity determination
process in humans and animals. Even cells from the oldest people may still
have some divisions left. Many scientists therefore believe that the biological
losses that precede the inability to replicate increase vulnerability
to disease and death well before the cells are incapable of further division.
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