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The Hayflick Limit is used to describe the number of times a normal cell will divide in its lifespan before undergoing [[Apoptosis|apoptosis]]. This number is usually between 40 to 60 times.<ref>Hayflick L. (1965). "The limited in vitro lifetime of human diploid cell strains". Exp. Cell Res.</ref><span style="line-height: 1.5em;">&nbsp;</span><span style="line-height: 19.9200000762939px;">This was proposed by Leonard Hayflick who described the life of a cell in three phases. Phase one is simply at the start when the cell is rapidly growing through healthy cell division. This is followed by phase two consisting of the slowing of mitosis. Finally, after a given time the cells reach phase three, where </span><span style="line-height: 1.5em;">[[Replicative cell senescence|senescene]]</span><span style="line-height: 19.9200000762939px;"> takes place. From here cell division stops and programmed cell death begins.</span><ref>Clark, J. (2014). Will the Hayflick limit keep us from living forever? - HowStuffWorks.</ref>  
The Hayflick Limit is used to describe the number of times a normal cell will divide in its lifespan before undergoing [[Apoptosis|apoptosis]]. This number is usually between 40 to 60 times.<ref>Hayflick L. (1965). "The limited in vitro lifetime of human diploid cell strains". Exp. Cell Res.</ref><span style="line-height: 1.5em">&nbsp;</span><span style="line-height: 19px">This was proposed by Leonard Hayflick who described the life of a cell in three phases. Phase one is simply at the start when the cell is rapidly growing through healthy [[Cell_division|cell division]]. This is followed by phase two consisting of the slowing of mitosis. Finally, after a given time the cells reach phase three, where </span><span style="line-height: 1.5em">[[Replicative cell senescence|senescene]]</span><span style="line-height: 19px"> takes place. From here cell division stops and programmed cell death begins.</span><ref>Clark, J. (2014). Will the Hayflick limit keep us from living forever? - HowStuffWorks.</ref><br>


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<span style="line-height: 1.5em">Immortality in a cell is impossible due to the shortening of the </span>[[Telomere|telomeres]]<span style="line-height: 1.5em"> on the </span>[[DNA|DNA]]<span style="line-height: 1.5em"> of the cells. During DNA replication, small segments of DNA at each end of the strands are lost after each </span>[[DNA replication|replication]]<span style="line-height: 1.5em"> as they are unable to be copied</span><span style="line-height: 1.5em">.</span><ref>Watson JD (1972). "Origin of concatemeric T7 DNA". Nature New Biol.</ref><span style="line-height: 1.5em">O</span><span style="line-height: 1.5em">nce the telomeres are depleted to such an extent it will result in apoptosis, a system used to prevent mutations.</span><ref>Eisenberg DTA (2011). "An evolutionary review of human telomere biology: The thrifty telomere hypothesis and notes on potential adaptive paternal effects". American Journal of Human Biology.</ref><span style="line-height: 1.5em">&nbsp;A&nbsp;</span><span style="line-height: 1.5em">cause for the telomeres shortening is oxidative stress</span><span style="line-height: 1.5em">.</span><ref>von Zglinicki T.(2002) Oxidative stress shortens telomeres.27(7):339-44.</ref>  


<span style="line-height: 1.5em;">Immortality in a cell is impossible due to the shortening of the </span>[[Telomere|telomeres]]<span style="line-height: 1.5em;"> on the </span>[[DNA|DNA]]<span style="line-height: 1.5em;"> of the cells. During DNA replication, small segments of DNA at each end of the strands are lost after each </span>[[DNA replication|replication]]<span style="line-height: 1.5em;"> as they are unable to be copied</span><span style="line-height: 1.5em;">.</span><ref>Watson JD (1972). "Origin of concatemeric T7 DNA". Nature New Biol.</ref><span style="line-height: 1.5em;">O</span><span style="line-height: 1.5em;">nce the telomeres are depleted to such an extent it will result in apoptosis, a system used to prevent mutations.</span><ref>Eisenberg DTA (2011). "An evolutionary review of human telomere biology: The thrifty telomere hypothesis and notes on potential adaptive paternal effects". American Journal of Human Biology.</ref><span style="line-height: 1.5em;">&nbsp;A&nbsp;</span><span style="line-height: 1.5em;">cause for the telomeres shortening is oxidative stress</span><span style="line-height: 1.5em;">.</span><ref>von Zglinicki T.(2002) Oxidative stress shortens telomeres.27(7):339-44.</ref>
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Latest revision as of 12:31, 20 October 2016

The Hayflick Limit is used to describe the number of times a normal cell will divide in its lifespan before undergoing apoptosis. This number is usually between 40 to 60 times.[1] This was proposed by Leonard Hayflick who described the life of a cell in three phases. Phase one is simply at the start when the cell is rapidly growing through healthy cell division. This is followed by phase two consisting of the slowing of mitosis. Finally, after a given time the cells reach phase three, where senescene takes place. From here cell division stops and programmed cell death begins.[2]

Immortality in a cell is impossible due to the shortening of the telomeres on the DNA of the cells. During DNA replication, small segments of DNA at each end of the strands are lost after each replication as they are unable to be copied.[3]Once the telomeres are depleted to such an extent it will result in apoptosis, a system used to prevent mutations.[4] A cause for the telomeres shortening is oxidative stress.[5]

References

  1. Hayflick L. (1965). "The limited in vitro lifetime of human diploid cell strains". Exp. Cell Res.
  2. Clark, J. (2014). Will the Hayflick limit keep us from living forever? - HowStuffWorks.
  3. Watson JD (1972). "Origin of concatemeric T7 DNA". Nature New Biol.
  4. Eisenberg DTA (2011). "An evolutionary review of human telomere biology: The thrifty telomere hypothesis and notes on potential adaptive paternal effects". American Journal of Human Biology.
  5. von Zglinicki T.(2002) Oxidative stress shortens telomeres.27(7):339-44.