FREE ESSAY ON APOPTOSIS AND AGING

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 [2001], 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 damage to the genetic
material results in a triggering of apoptosis (Schneider 67). The length of the telomere
string is what limits the number of times the particular cell can divide, and by passing
this information on to it's issue, similarly limits any descendants to similar division.
This is the safety mechanism that prevents normal cells from growing out of control and
becoming a malignancy. Failure of this safety mechanism is what is seen in cells of
breast cancer tumors (Cech). 
The telomere theory is only one of many that allege controls over the apoptotic
processes, but is the leading focus of research for cancer centers through out the world.
Other leading theories include, hormonal control, and protein signaling devices, referred
to as "factors", a term often associated with compounds of either unknown origin or
affect (Leeuwenburgh 2.0, Cotran 76, Cech). 
Some common threads do exist among apposing theorists, in particular; the very genes that
may hold the keys to eternal life, are the genes that allow cancer to spread. If these
genes are disabled cancer is the result. Apoptosis, as stated, is the natural regulatory
mechanism by which cancerous cells would be eradicated. 
In order for our technology to achieve control over this phenomenon, we must first learn
to control our leading killer today, cancer (Cech). After careful scrutiny of the latest
research, as detailed herein, this technology is beyond our present grasp. Some day soon,
we may find the keys to unlock the mysteries to our own genetic code, but what then will
we do with it? Who we really wants to live forever?
Bibliography
Works Cited
Adamchak, L. Personal interview. 10 April, 2001
Agin, D. P. ed. "Molecular Biology: Apoptosis." Science Week Focus Report. 
1 March, 1999, U. of Chicago, 19 March, 2001, .
Bank, Lew, et al. The Genetics of Aging. Schneider, Edward, L. New York: Plenum Press,
1978
Cech, T. "Life at the End of the Chromosome: Telomeres and Telomerase." 20 Sept. 2000,
National Institute on Aging, NIH Massur Auditorium, 18 March, 2001. .
Cotran, Tucker, and Vinay. Robbins Pathologic Basis of Disease 6th ed. Philadelphia:
Saunder, 1999
Heydari, Ahmad, R. Understanding the Secrets of Aging and Cancer Through Nutritional
Intervention. 3 January, 2001, Heydari Laboratory, Wayne U., 
19 March, 2001, .
Leeuwenburgh, C., Pollack, M. Mitochondrial control of Apoptosis in Aging and Exercise.
21, January, 1999 Aging Biochemistry Laboratory, College of Health and Human Performance,
U. of Florida, 19 March, 2001, . 
Martini, Frederic, H. Fundamentals of Anatomy and Physiology. 4th ed. New Jersey: 
Prentice Hall, 1998
Sinha, G. "Our Genes Exposed." Popular Science. May 2001: 43