Telomere Length
The Hayflick limit has been found to correlate with the length of the telomere region at the end of a strand of DNA. During the process of DNA replication, small segments of DNA at each end of the DNA strand (telomeres) are unable to be copied and are lost after each time DNA is duplicated. The telomere region of DNA does not code for any protein; it is simply a repeated code on the end region of DNA that is lost. After many divisions, the telomeres become depleted and the cell begins apoptosis. This is a mechanism that prevents replication error that would cause mutations in DNA. Once the telomeres are depleted, due to the cell dividing many times, it will no longer divide having reached its Hayflick limit.
This process does not take place in cancer cells due to an enzyme called telomerase. This enzyme maintains telomere length, which results in the telomeres of cancer cells never shortening. This gives these cells infinite replicative potential. A proposed treatment for cancer is the usage of telomerase inhibitors that would prevent the restoration of the telomere, allowing the cell to die like other body cells. On the other hand, telomerase activators might repair or extend the telomeres of healthy cells, thus extending their Hayflick limit. Telomerase activation might also lengthen the telomeres of immune system cells enough to prevent cancerous cells from developing from cells with very short telomeres.
Carnosine can increase the Hayflick limit in human fibroblasts, and also appears to reduce the rate of telomere shortening.
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