Hayflick limit
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The Hayflick limit is the number of times a cell will divide before it stops due to the telomere reaching a critical length.[1]
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[edit] Overview
The Hayflick limit was discovered by Leonard Hayflick in 1965, at the Wistar Institute (Philadelphia), 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; for example, the cells of some long-lived sea-birds such as Leach's Petrel are technically immortal.[2]
This telomere lengthening 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 the DNA end will be marked as a DNA double-strand break. Telomere shortening together with telomerase activation is one of the most prevalent aberrations in pre-cancerous lesions. [3]
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[clarification needed]. These methods are also used by cancer cells to divide uninhibited.[citation needed]
The normal Hayflick limit of cells in organisms other than humans varies and affects their life span.[citation needed]
Carnosine can increase the Hayflick limit in human fibroblasts,[4] as well as appearing to reduce the telomere shortening rate.[5]
[edit] See also
[edit] References
- ^ Hayflick L. (1965). "The limited in vitro lifetime of human diploid cell strains.". Exp. Cell Res. 37 (3): 614–636. doi:. PMID 14315085.
- ^ *Haussmann M. F. et al. (2003): Telomeres shorten more slowly in long-lived birds and mammals than in short-lived ones. Proceedings of the Royal Society of London B: Biological Sciences, 270:1387–1392
- ^ Scientific article in currented paper: Telomere length, telomeric proteins and genomic instability during the multistep carcinogenic process - http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T5S-4RV1JRM-1&_user=640931&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000034278&_version=1&_urlVersion=0&_userid=640931&md5=4eefbac73f5f54e9c908a79f0dacef15
- ^ McFarlan GA.; Holliday R. (1994). "Retardation of the senescence of cultured human fibroblasts by carnosine". Exp. Cell Res. 212 (2): 167–175. doi:. PMID 8187813.
- ^ Shao L; Li QH, Tan Z (2004). "L-carnosine reduces telomere damage and shortening rate in cultured normal fibroblasts.". Biochem Biophys Res Commun. 324 (2): 931–936. doi:. PMID 15474517.
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