Multicellular organisms have three compartments


Multicellular organisms have three compartments in which ageing affects; dividing cells (such as cells of the skin and kidneys), non-dividing cells (cardiac and skeletal muscle cells), and acellular cells (such as bones hair and teeth).Aging sometimes affects all of these, whilst some mechanisms of ageing only affect one of them.

Replicating cells are more common in long lived organisms, and are present for growth and repair of important tissues, which in turn contributes to their longevity. Nevertheless these cells are very susceptible to cancer.

Cellular senescence is described to be when normal somatic cell looses it ability to divide.

To find out whether ageing was a cellular process or an organismal process, Alexis Carrel cultured chick myocytes. He hypothesised that all cells explanted in culture were immortal; which was supported by the fact that he cultivated chick myocytes which grew for 34 years. This proved that ageing was in fact an organismal process not a cellular process.

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Other scientists were led to believe this was true, but no one else could replicate these results in their own experiments. This was because Carrel was wrong and he had made an error in his original experiments. His error was that he probably contaminated the culture with live cells, which n turn continued to keep he culture going for 34 years.

In 1961, Leonard Hayflick discovered that cells were not immortal. He was preparing normal cells to be exposed to cancer cells when he discovered that the normal cells had stopped proliferating. At first thought, Leonard thought it was due to a mistake made by him, but then he came up with the idea that the cells had stopped proliferating because they has some kind of cell counting mechanism.

To further investigate this idea, Leonard Hayflick along with Paul Moorheed, designed an experiment to show how normal cell division really worked. In this experiment, cells were isolated from human tissue and were placed n a vessel containing nutrient medium. The cells were left to divide ad for a confluent layer on the surface of the vessel. When this happened, half of the cells were discarded and the remaining cells were allowed to grow again in the medium. This was called the first passage.

This process was repeated until the replication of the cells is lowed down and stopped, this was seen after 50 +/- 10 passages. At this point, the cells were said to have reached the Hayflick limit, and have reached replicative senescence.

It was then proposed that this cellular senescence contributed to the ageing processes.

Early studies suggested that the was a correlation between cellular senescence and organismal ageing ( Rhome 1981). Rhome showed that there was a correlation between the maximum species lifespan and in vitro cell doubling limits. This was evidence to support that there was a Correlation between relationship between longevity of mammalian species and life spans of normal fibroblasts in vitro.

But further studies showed that this was not the case. Antonello Lorenzini et al (2005) proved that the replicative capacity doesn't correlate with lifespan but with body mass.

In this investigation the relative life-span of fibroblast of the cultures from 9 species were compare with their longevity and the body mass. All the donors were healthy at the time of the biopsy and were approximately in the young adult range.

The mean proliferative capacity was compared with the maximum species longevity and the mean adult body mass from each species. The results indicated that a species' replicative capacity is primarily a function of adult body size rather than longevity.

Another experiment was carried out to investigate if the replicative capacity of cells decreases with age? The initial results indicated that this was true, as the number of doubling before cellular senescence decreased with age. But these results included unhealthy donors, such as donors with diabetes. The rate of telomere shortening in people such illnesses s accelerated. In addition biopsies from cadavers were used.

If these results were removed, leaving only the healthy donor results, then the correlation between the two disappeared, once again show no real correlation between ageing and the replicative capacity of the cells.

In order to understand whether cellular senescence can contribute to ageing, the mechanism of which cellular senescence occurs must be looked at.

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Alexey Olovnikov (1966) proposed mechanism for Hayflick limit in his marginotomy theory, based on the end replication problem. When the lagging strand of DNA is replicated, the primers are degraded and Okazaki fragments are left behind. These fragments are ligated. The Problem with the replication of the lagging strand is that there is a need for RNA primer. The end part of the chromosome cannot e replicated properly therefore Chromosome ends will get shorter each round of division. Telomeres were then used to cap the ends of the chromosomes.

Experiments done by Bodnar et al (1998) showed that telomerase was important in the proliferation of cells. In this investigation they expressed human telomerase in normal human somatic. By doing this cellular senescence was stopped and it resulted in cellular immortality

The length of Telomeres in mitotic cells are very heterogeneous, this is because they are very sensitive to oxidative damage. This also explains why mitotic cells in cell cultures don't age at the same time. This was further proven by Thomas von Zglinicki (2002) using the cellular sentinel model. In this investigation he showed that telomere shortening was an indicator of accumulated genomic damage.

It is very impotent that DNA damage is made to exist the cell and turn the telomerase off because telomerase s expressed in cancer cells as well as other type of cells.

Cancer, the growth of abnormal cells by uncontrolled cell division, is caused by activating mutations in proto-oncogenes and loss of function mutations in tumour suppressor genes). Cancer is a disease of ageing as the occurrence of cancer increases with age.

Absence of telomerase in most mitotic cells limits proliferative capacity, protecting against cancer. Cellular senescence is tumour suppressor mechanism.

There are two views to whether ageing causes cancer. The first view was that a lot of mutations are required to make a normal mitotic cell cancerous. So over time there is n accumulation on mutations, therefore at later age you will see the result of the mutation accumulation explain the increased cases of cancer in older people. The other view is that it accelerates the development of cancer. The changes in the environment of the cell causes mutated cells more likely to become cancerous cells.

An investigation by Krtolica et al 1999 showed a link between cancer and aging. In this experiment young and senescent cells were taken and cultured with tumour cells upon them. The results showed that the tumours grew faster on senescent cells than on the normal young cells.

In addition, in other experiment they injected some mice with tumour cells and young cells, and other mice with tumour cells and senescent cells. It was seen that the mice with the tumour cells and senescent cells had a higher chance of developing tumours than the mice with the younger cells. The conclusion from this is that, senescent cells promote cancer formation.

From all this information, a mechanism for cellular senescence was formed. It was proposed that cellular senescence alters the pattern of gene expression, and therefore changes in the secretion of growth factors that degrade the extracellular matrix. The Senescent cells alter the cellular microenvironment of the cell, making it carcinogenic. Campisi, J. (2005)

Cellular senescence seems to protect younger individuals from cancer, which enhances their fitness. These cells accumulate over time to a large amount at an older age, which then promotes the formation of carcinogenic cells and cancer.

This seems to follow the evolutionary theory of ageing as the thing that promotes fitness at a younger age has negative effect when the individual gets older. This is an example of antagonistic Pleiotropy.


  • Campisi, J. (2005) Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. Cell 120, 513-22.
  • Krtolica, A. and Campisi, J. (2002) Cancer and aging: a model for the cancer promoting effects of the aging stroma. Int J Biochem Cell Biol 34, 1401-14.
  • Dimri, G.P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E.E., Linskens, M., Rubelj, I., Pereira-Smith, O., et al. (1995) A biomarker that identifies senescent human cells in culture and in aging skin in vivo. Proc Natl Acad Sci U S A. 92, 9363-9367.
  • Krtolica, A., Parrinello, S., Lockett, S., Desprez, P.Y. and Campisi, J. (2001) Senescent fibroblasts promote epithelial cell growth and tumorigenesis: a link between cancer and aging. Proc Natl Acad Sci U S A 98, 12072-7.
  • Lorenzini, A., Tresini, M., Austad, S.N. and Cristofalo, V.J. (2005) Cellular replicative capacity correlates primarily with species body mass not longevity. Mech Ageing Dev 126, 1130-3.
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