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Telomerase Do We Want To Live Forever

Telomerase: Do We Want To Live Forever Essay, Research Paper Telomerase: Do we want to live forever I. Introduction There have been countless technological breakthroughs in this century. Some have made life in the entire world a better place, while some have surely proved to be devastating. Could someone a hundred years ago have imagined how a contraption like the telephone could change the course of history; that a person could be on one side of the world and in another seven hours later; the idea that a man could walk on the moon would have cost us our heads in other times.

Telomerase: Do We Want To Live Forever Essay, Research Paper

Telomerase: Do we want to live forever I. Introduction There have been countless technological breakthroughs in this century. Some have made life in the entire world a better place, while some have surely proved to be devastating. Could someone a hundred years ago have imagined how a contraption like the telephone could change the course of history; that a person could be on one side of the world and in another seven hours later; the idea that a man could walk on the moon would have cost us our heads in other times. As we come forward in our science fiction technological advances, the human race is presented with the prospect of immortality. Finally some light has been shed on dying and the factors that contribute to it. By understanding some basic concepts, we can begin to understand that there are ways we can avoid an early death. Plenty of research has been conducted on the subject, but until recently, new breakthroughs have shown us some concrete evidence. An enzyme exists in our body that has the potential for extending our individual life expectancies. The name of this enzyme is telomerase. Before understanding how this enzyme can help us postpone death, we have to first examine the reason that normal body cells die. II. Why cells die There are two kinds of cells in humans. These are somatic cells and gametes. Most of our somatic cells undergo a process called mitosis. In which it is believed that one cell divides into two identical daughter cells. It is also a well known fact that the resulting daughter cells have the same number and kind of chromosomes as the original parent nucleus. This is not entirely true. Every time one divides, it sheds tiny snippets of RNA known as telomeres, which are a part of the DNA sequence. Telomeres serve as protective caps on the ends of chromosomes. After perhaps fifty divisions, a cell’s telomeres become so truncated that its chromosomes begin to fray. This only occurs in somatic cells that reproduce and not in other cells like nerve cells that do not normally reproduce. A popular analogy states that these telomeres are like shoelaces that have lost their plastic coverings at the ends. Our cells can detect when a telomere is too short, and eventually stops dividing and dies off. It is not yet known how cells sense their shortened telomeres. The number of divisions varies between 40 and 90, depending on cell type, and is known as the Hayflick number, after Leonard Hayflick, who discovered this phenomenon in 1965. Another factor that contributes to the death of cells is the over-stimulation of cell divisions. A restrictive diet has proven to elongate the life of cells also. Since eating less food provides less materials for cell reproduction, we can delay cell divisions. Eating too little may result in the opposite as the stresses of malnutrition on the body could kill off healthy cells. Helping the cells in our body divide at a slower pace makes sense, since less telomeric material will be lost. But balancing a restrictive diet that won’t have unhealthy results could prove a challenge. III. Telomeres and Telomerase Telomeres are highly conserved sequences of RNA that are present at the ends of chromosomes and consist of repeats of the nucleotide sequence TTAGGG. These nucleotide sequences shorten every time a cell divides. At birth, telomeres consist of about 15,000 base pairs of repeated TTAGGG DNA sequences. Every time a cell divides it loses 25-200 DNA base pairs off the telomere ends. Once this pruning has occurred about 100 times a cell senesces (or ages) and does not continue dividing. Cellular senescence is the limited capacity of cells to divide beyond a finite number of population doublings (finite growth potential). Germ cells like ova and sperm cells maintain there telomere length at a maximum length because they have an active enzyme called telomerase in them. Bacterial cells also have an active telomerase enzyme giving them unlimited cell divisions. Normal body cells do not make telomerase. Telomerase is an enzyme that repairs damaged telomeres. Most human cells stop making telomerase early in life and, therefore, create A biological clock that kills us in our 70’s and 80’s. Cellular immortalization refers to cells that are capable of indefinite proliferation (or unlimited lifespan). In long lived multicellular organisms, immortality may be thought of as an abnormal escape from cellular senescence. There is a connection between cancer and the effects of telomerase. There is a gene in chromosomes of all somatic cells in the human body that is designed to produce telomerase. But in order to produce it, that specific gene must somehow be activated. We don’t know how this occurs yet, but in most cancer cells telomerase is present. This means that normal cells can mutate into cancer cells as a normal biological event. If the telomerase gene is not activated the mutated cell will eventually run out of cell divisions and die off. But if the mutations involve the activation of telomerase, these mutant cells can soon turn into tumors and cancer.

VI. Cell fountain of youth In a paper published in the journal Science, January 16, 1998, scientists explain that the introduction of an active telomerase gene into normal mortal cells resulted in the lengthening of telomeres and a marked increase in the life-span of the cells, making the cells potentially immortal. What’s more important, the cells turned out normal and healthy, not cancerous, as expected by some critics. VI Actual research about telomerase Support for the telomeric theory of aging is seen in the disease progeria, a rare disorder of accelerated aging. Children with this disease die in early to middle childhood with bodies of 90 year olds. Their telomeres are a lot shorter than those of normal humans. The progressive shortening of telomeric DNA had long been thought of as the molecular clock of cell aging, but until now, direct evidence has been elusive. The researchers at the University of Texas Southwestern Medical School in Dallas and scientists at Geron, a biotechnology firm in California, resolved the controversy by introducing telomerase, the enzyme which elongates and rebuilds telomeres, into cells which normally lack it. Telomerase is normally found in germline cells such as sperm and ova, as well as in several cancers, but is absent in normal somatic cells. Foreskin fibroblasts and retinal epithelial cells were transfected with the gene for telomerase and were able to use it to prevent telomere shortening and cell death. Whereas control cell lines underwent their normal number of divisions and then stopped and died, cells expressing telomerase continued to divide. Normally cells stop dividing after about the 70th generation. These cells are now up over 100 population doublings. Moreover, they look like young cells under a microscope, and molecular tests suggest they are biochemically “youthful.” This researched can be sumed up in the following sequence: 1 In cells where telomerase is absent, telomeres shrink with each cell division.2 After enough divisions, telomeres become dangerously short.3 Cells with very short telomeres stop dividing and die.4. By adding telomerase, researchers have been able to stabilize the telomeres, ensuring the cells can divide indefinitely. Custom making tissues One possibility would to be to grow bone marrow for transplant from a persons own cells. Currently this can’t be done since the cells reach their senescence before they have produced enough cells to transplant. The application of telomerase may allow these cells to continue growing to provide sufficient cells for transplant purposes. Scientists speculate that the work will have applications in reversing macular degeneration, a common cause of blindness, in which central retinal cells die. The findings may also allow doctors to accelerate wound healing, extend the viability of rare tissues, grow skin for burn victims, and combat some forms of arteriosclerosis. Custom making organs In arthritis stricken patients, a biopsy could be taken and telomerase could be used to grow “sheets” cartilage that could then be reinserted into the joints afflicted. In heart attack victims part of the heart becomes necrotic. Meaning that the some tissue dies off. Growing cardiac muscle cells in a lab would not be a problem. The removal of the necrotic tissue and the implantation of the new tissue would certainly give the heart an advantage. Neural implications Since nerve cells do not divide in human adults, there will not be much we can do for diseases of the brain, spinal chord, and nerves with regards to telomerase. Our ability to keep our nervous system in shape will be the only boundary that would keep us from living forever. We can certainly keep our minds healthy for more than 80 to 100 years. Unless we can replace our brains, we really can’t bridge the gap to eternity. VIII. Conclusion In conclusion, the next big thing since the discovery of nuclear energy will be a way to help humanity live longer, healthier lives. Telomerase and its miraculous qualities will by no means grant us eternal life. It will literally do away with nursing homes and recovery centers. Almost everybody will have access to a better way of life. REFERENCES:C. Greider and E. Blackburn (Feb 1996) Scientific American 80-85 Shay JW: Aging and cancer: Are telomeres and telomerase the connection? Mol Med Today 1:378-384, 1995. Deborah Josefson : US scientists extend the life of human cells ; BMJ No 7127 Volume 316 News Saturday 24 Janu37 Norton, JC, Piatyszek, MA, Wright, WE, et al:Inhibition of human telomerase activity by peptide nucleic acid oligomers. Nature Biotech 14:615-619, 1996. Bryan TM, Englezou A, Gupta J, et al: Telomere elongation in immortal human cells without detectable telomerase activity. EMBO J 14:4240-4248, 1996.ary 1998 Langford, LA, Piatyszek, MA, Xu, R, et al: Telomerase activity: A prognostic indicator in ordinary meningiomas. Human Path (in press, 1997). Hiyama E, Hiyama K, Yokoyama T, et al: Correlating telomerase activity levels with human neuroblastoma outcomes. Nature Med 1:249-255, 1995. Kim, N-W, Piatyszek, MA, Prowse, KR, et al: Specific association of human telomerase activity with immortal cells and cancer. Science 266:2011-2015, 1994.

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