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Apoptosis and Aging
When we gain control of the gene responsible for the phenomenon of apoptosis, we will be in control of aging.
We are finding more evidence every day, indicating genetic links to all sorts of factors in the human being. We are just now beginning to scratch the surface of our own genetics. A landmark discover has just been unveiled:
In February , the two groups charting the human genome published their results—the entire 3 billion base pair sequence. The only definitive conclusion so far: Humans are far more complicated than we thought. …Eric Lander, director of the Whitehead Center for Genome Research in Cambridge, Massachusetts … adds: “within a decade, we will understand a lot about the causes of diseases. Understanding, however does not translate into cures.” (Sinha 43)
With this research we will uncover more factors that our genetic code regulates, many factors that were previously believed to be random events. Spontaneous cell death, as it turns out is not spontaneous at all, but genetically predetermined at conception.
Cell death is an essential part of life. The cells in our bodies are constantly dividing, producing hundreds of thousands of new cells every second. To maintain balance, for every new cell, another cell must die. Our cells are programmed to kill themselves through a process called apoptosis. This in-built program of cell suicide prevents cancer by eliminating cells with damaged genes (Cotran 18). Similarly, our bodies replace cells with a new type of cell when a change is needed, such as during embryonic development (Cotran 18). To illustrate this point, we look at one of Dr. Adamchak’s “stories of physiology,” as taught from Martini, when a bone is being formed cartilage cells, or condrocytes, come into an area to build a cartilage model of the bone. Once this model of bone is complete, the cartilage cells are given the command to die. Osteoblasts, or bone building cells, move in to the space formerly occupied by the Condrocytes, and replace the cartilage matrix with a Calcium rich, rock hard, matrix, we know as bone (188). In the foregoing example there are instances of cells being told to die, this is programmed death, and known as apoptosis.
During life, our cells carry out metabolic functions, producing digestive enzymes and waste products, which are harmful to surrounding cells, if it spewed into the fluids among the cells. These enzymes and toxins must be packaged in a way that is not harmful to the interstitial environment, and in a manner in which appropriate cells in the region can readily absorb them. This must be done without invoking an inflammatory response (Browder).
Aging, also known as Senescence, is a natural process, “beginning at reproductive fitness and culminating in death,” Observed in most living organisms, senescence is characterized by a gradual reduction in “reserve capacity of organ systems”, (Heydari). Supporting research by U. of Florida’s Aging Biochemistry Laboratory indicates an increased apoptotic rate of cardiomyocytes, T-lymphocytes, and neurons, as age advances (Leeuwenburgh, par. 3.1). These factors manifest the classic signs of aging as well as many age-associated diseases, such as reduced cardiac function, susceptibility to illness and neurological disease (4.0).
Apoptotic cell death is only one factor of the aging mechanism. Normally, during development, as cells are “deleted” new cells are made to occupy the void. As an organism ages the number of dividing cells declines, resulting in a decreased capacity to heal. Every high school student knows that as cells divide, DNA is unzipped and re-zipped during the copying process. This process, by which we grow and heal, is believed to be responsible for our senescence.
Without some form of error correction, manipulation of DNA will result in damage to the codes contained in it. Error correction is provided by “The stuff at the end” of each chromosome string, as it literally translates from Latin, is known as a telomere (Cech). The telomere, a short string of amino acids, contains the error correcting information required to properly duplicate DNA, however with each unzip the telomere becomes shorter, until it is gone. The absence of the telomere results damaged DNA, thus triggering apoptosis (Agin, Cech). DNA can also be damaged by exposure to forms of radiation including ultra-violet radiation from the sun. As stated any
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Gerontology, Apoptosis, Cellular senescence, Cell signaling, Immunology, Ageing, Mechanistic target of rapamycin
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