The Hayflick limit is the number of times a cell will divide before it stops due to the telomere reaching a critical length ^[1].

It was discovered by Leonard Hayflick in 1965, at the University of California, San Francisco (UCSF), when Hayflick demonstrated that normal human cells in a cell culture divide about 52 times in 20% oxygen (i.e. practically normal air) or 70 times in 3% oxygen (which is the same as human internal conditions). It then enters a senescence phase (refuting the contention by Alexis Carrel that normal cells are immortal). Each mitosis shortens the telomere appendix on the DNA of the cell, thus ticking back an "inner clock" for each subsequent copy of the cell. Some organisms' cells do not encounter the Hayflick limit due to telomere lengthening, examples are long-lived sea-birds, whose cells are technically immortal.

This mechanism is believed to have evolved primarily to protect the body from creating a potentially-cancerous cell. Because of the fragmented way DNA replicates, a very short telomered cell may lead to genomic instability when the proteins meant to be located on the telomere will fail to attach and it will be marked as a double-strand DNA break, possibly leading to cancer.

Many stem cells, as they are undifferentiated, are not affected by the Hayflick limit. They exist in every tissue and may continue reproducing for the lifespan of the organism. To avoid reaching the barrier, cells that need to keep on dividing express the telomerase enzyme or use Alternative Lengthening of Telomeres mechanism. These methods are also used by cancer cells to divide uninhibited.

The normal Hayflick limit of cells in organisms other than humans varies, and affects their life span.

Carnosine can increase the Hayflick limit in human fibroblasts^[2]. It appears to reduce the telomere shortening rate as well ^[3].

See also

• Apoptosis
• Biological immortality
• HeLa cells

External links

Cell immortality and cancer

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