Aging Processes Leading To Cell Death Biology Essay


People always question how and why they age. What is happening inside the bodies to bring on the wrinkles and allow the muscles to weaken? How do cells die? In recent decades, scientists have made great advances in understanding the processes of cell aging and cell death. They have found that, when carefully controlled, cell death is critical to life. Without it people would not have hands or the proper brain cell connections to be able to read and communicate. Some of the most easily observed age-related changes in humans are found in the skin. Theories have been divided between the programmed and stochastic theories. Programmed theories imply that aging is regulated by biological clocks operating throughout the lifespan. This regulation would depend on changes in gene expression that affect the systems responsible for maintenance and defence responses. Stochastic theories accuse environmental impacts on living organisms that induce cumulative damage at various levels as the cause of aging.

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Damage to each person's genome, accumulates with time. Some DNA (Deoxyribonucleic acid) mutations arise from errors in the copying of DNA as well as from external sources. DNA mutations are known to cause cancer and also may contribute to cellular aging. One of the assumptions in biology is that normal cells can go through only a fixed number of divisions before they die, a process called senescence. Many scientists wonder that another way to the aging process is the build up of cellular retirees. It's been discovered that when the cells divide more than 60 times they tend to lose their power to replicate. Then they eventually stopped dividing and die. Before a cell divides, it copies its chromosomes so that each daughter cell will get a complete set. Sometimes the copying occurs in the wrong way, the very end of our slender chromosomes don't get copied. As a result, the chromosomes get shorter with each cell division. Fortunately, the telomeres remove all the unwanted things in the cell so no harm comes from leaving parts of them behind. But once a cell's telomeres shrink to a critical minimum size, the cell stops dividing (Spence, Alexander P. 1995).

During mitosis, the cell duplicates its DNA and divides to form two daughter cells. Cell division is responsible for the replacement of the cells that line our respiratory tracts. When it comes to cell death, we now know that a cell can die by a process known as apoptosis. Every year the average human looses half of their body weight in cells via apoptosis. Apoptosis is the term used to describe how cells die under a range of physiological and pathological circumstances. Apoptosis is a fundamental process that cuts across the boundaries of many scientific disciplines. It is of interest to the immunologist, because of its role in cell deletion in the immune system and the deregulation of the process seen in a number of autoimmune diseases and AIDS. To the cancer biologist, apoptosis not only appears to contribute to the development of some cancers, but also hinders their treatment when cells become resistant to apoptosis and are not killed following drug treatment. Developmental biologists also have a keen interest in the process because of the programmed loss of cells which occurs via apoptosis during tissue sculpting and is part and parcel of embryonic development.

People with Werner syndrome accumulate (a premature aging disease that begins in adolescence or early adulthood and results in the appearance of old age) excessive DNA mutations because this repair enzyme is either missing or not working properly. A few years after the discovery of the human Werner syndrome gene, scientists identified a corresponding gene in yeast. Removing the gene from yeast cells shortened their lifespan and led to other signs of accelerated aging. This supports a link between this gene and aging, and it provides scientists a model with which to study Werner syndrome and aging in general. An article of Aging and development(1997) entitled Cell aging in vivo and in vitro, presents evidence that cells accumulate damage over a lifetime which results in gradual loss of differentiated function and growth rate. In 1972, Andrew Wyllie and colleagues published a paper that described the cell death process of apoptosis. In the mid to late 80's, immunologists and developmental biologists rediscovered the 1972 paper of Wyllie and began to explore the underlying biology of apoptosis in both immunological and development systems. The 90's have seen an explosion in the number of papers devoted to cell death. Scientists have realized that cell death via apoptosis is a fundamental biological process, which we know very little about. It is the damage to cells over a lifetime that stimulates the effects of aging, which induces a gradual loss of differentiated function of the cells and growth rate. This stress (e.g. biochemical damage) on the cells reduces its capacity to multiply. It is not related to changes in hormonal states, blood flow or other system effects of aging. This is an important distinction for researchers to make in understanding what is aging (De Felici, M. and M. Pesce. 1994)

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Programmed cell death, is an important mechanism in both development and homeostasis in adult tissues for the removal of either a superfluous, infected, transformed or damaged cells by activation of an intrinsic suicide program. Cells undergoing apoptosis usually exhibit a characteristic morphology (The branch of biology that deals with the form and structure of organisms without consideration of function). Inhibition of cell death might contribute to ontogenesis by promoting cell survival instead of death. Likewise, triggering cell death might provide the means for eliminating unwanted cells (e.g., tumour cells). This might be accomplished by harnessing tumour necrosis factor (TNF), which triggers apoptosis in some target cells. However a disadvantage to the organism of the mechanism that necessitates signalling to prevent apoptosis is that its failure by mutation can lead to the survival of unwanted cells which, paradoxically, can lead to death of the organism itself. On the other hand, an opportunity is presented by such a mechanism to allow investigators to devise means for targeting unwanted cells for destruction (Barinaga M. 1996).

Therefore, the idea of a death process has stirred a lot of interest. The quest to discover why and how a cell switches on its death programmed is one of the most interesting areas of biology because if we can understand the process by which a cell kills itself, we may be to able to interfere and either prolong the life of the cell or speed up its death.