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The Biology of Aging

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The Biology of Aging

Introduction

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Aging is an intricate multifactorial process which generally influence by the genes and the environment (Arking 11). Although both physiological and molecular basis of aging have not yet fully understood, the identified genetic factors in the near future may shed light on the underlying mechanism in aging. The physiological and biological bases of aging measurements revealed the prevalent changes brought by the complex processes (Arking 11). These changes in the tissue, molecular and cellular organizations affect the entire organ system of an animal.

Most of these changes involve molecular mechanisms that cause cellular damage which in turn can adversely affect the individual. Hence, aging is generally described as a sequence of time-dependent changes which increase the probability of death as the organism gains progress in age (Macieira-Coelho 3). On the other hand, death is a prominent characteristic of biological aging. The increasing tendency for death is largely imparted by the genes or gerontogenes which gave different life span for various animal species (Arking 5).

Further, life threatening factors from the environments like predation and diseases aggravate the fatality rate of the immortal organism. Thus, the main effect of genes on aging is not merely on the aging attributes; rather it is a non-adaptive process wherein the gerontogenes may either have no effect on the fitness of the organism or may probably give benefits only at the early stage of life. In addition, genes are not chosen by the nature to speed up the aging process; aging is the result of the absence of selective pressure for the organism’s late period of life.

The Cell Death

Cell death is either triggered by necrosis or apoptosis and differentiated based on morphological and biochemical changes undergone by the cell (Schulze-Osthoff 2). As such, plasma membrane of the cell may suffer necrosis due to extreme physiological conditions like hypothermia and hypertonic environment. This plasma membrane damage can also be induced by pathological agents and viruses. On the other hand, the cell can incur apoptosis even at normal physiological conditions, thus, often called as “programmed cell death” or “cellular suicide” (Schulze-Osthoff 2).

The “programmed cell death” involves intricate biochemical processes; pathogens and environmental stresses attack every cell by means of chemical signals. For example, death signals can be originated from malfunction in DNA repair mechanism, cytotoxic drug treatment, ligation of cell surface receptors, and irradiation (Gewies 4). In relation to this, the cell responses to inhibit pathogenic growth and disease development by means of protective genes activation which in turn, through chemical reactions, kills the infected cells. The cellular death process then is directed by specific signals and independent biochemical processes in every cell. Hence, understanding the intricacy of cell death requires an intensive knowledge on chemical principles behind apoptotic or necrotic process.

Theories of Biological Aging

The biological theories of aging are generally grouped into stochastic and non-stochastic. Stochastic theories are based on the events’ random accumulation while the non-stochastic delves on predetermination (Woodrow 15). Stochastic events include free radicals, error, somatic mutation, genetics, cross-linking of proteins, cellular wear and tear. On the other hand, non-stochastic involves biological clock, neuroendocrine, and immunology.

The Wear and Tear Theory

The wear and tear theory holds that just like ordinary objects, the constant exposure of cells to aging factors would result to the accumulation of cellular damage which may eventually lead to cell death (Woodrow 17). Cellular damage can be instigated by deficiency, intoxication or trauma. The deficiency of any physiological substance needed by the cell will result to cellular malfunctions (Woodrow 20). In particular, the cell needs nutrients and oxygen for its metabolism. The insufficient supply of oxygen turns aerobic metabolism into anaerobic and consequently leads to inefficient production of energy. In fact, anaerobic metabolism can only produce two ATP molecules for every gram of glucose as compared to thirty-eight ATP molecules produced under aerobic process (Woodrow 20). To sustain the energy needed by the cell under anaerobic process, the rate of metabolism will be elevated that will generate higher waste product quantities. These waste products must be removed from both intracellular and extracellular environments in order to prevent cell poison. Meanwhile, in the time of inadequate glucose supply, the mitochondria use fats to produce energy. As similar with the anaerobic process, the catabolism of fats generates greater waste quantities.

The obstruction of cellular function causes intoxication. Toxins are either produced by the body or exogenous. Exogenous toxins, triggered by biological and non-biological species, produce chemicals such as interleukins, free radicals and tumor necrosis factor alpha that damage cells (Woodrow 20). On the other hand, trauma refers to the cell’s physical injury. The cell experiences trauma due to either internal or external pressure. For instance, a virus can penetrate and reproduce inside the cell which eventually results to membrane rupture because of viral population. The viral release into the neighboring cells leads to cellular invasion and the cycle repeats all over.  In addition, cellular trauma can be stimulated by the external conditions of the cell such as hyperthermia, radiation and hypothermia as well as mechanical pressure on superficial tissue.

Genetic Theory

For genetic considerations, longevity studies that were conducted on twins showed that approximately 25% of the differences in the life span of humans can be ascribed to genes (Chadwick and Goodie 135). As well, the genes of the centenarian populace were assessed. Researches found that specific genes like APOE prolong the life-expectancies of the centenarians while some human genes were found to cause premature aging (Chadwick and Goodie 135). For instance, the gene involved in the Werner’s syndrome induces the early signs of aging in adults such as atherosclerosis, graying and loss of hair, muscle loss and heart valve calcification. Nevertheless, the main goal of human aging studies is not on life span impact but its effects on health.

Free-Radical Theory

Oxygen radicals are reactive chemical species that trigger oxidative degradation to cellular organelles and biomolecules including the DNA and the lipid bilayer of the cell membrane (Macieira-Coelho 14). These oxygen radicals are naturally generated by the cells due to oxidative metabolism specifically in the mitochondria, the power house of the cells. A number of studies have successfully directly linked oxygen radicals to cellular damage (Macieira-Coelho 14). As such, it was theorized with the amassing of tissue and cellular degradation, the rate of aging is tantamount to the rate of oxidative damage accumulation. Meanwhile, every organism has cellular defense that neutralize the effects of the oxidative reactions. This cellular defense is created by the synergetic approach of different molecular species which include enzyme and other antioxidants that convert the free radical oxygen into a non-toxic form.

The Biological Clock

Even though the great advancement in medicine has prolonged life and reduced the rate of mortality, the inevitable course of aging and death is still at hand. In 1985, Hayflict reported that the mitosis of the normal embryonic cells of humans undergo at most 50 cell divisions. Thus, the life of cell is finite and controlled by a “chronometer” or a “pacemaker” inside every cell (Hayflict 21). In 1994, telomerase, an enzyme, was found as protector of chromosomal telomeres from degradation ( Woodrow 23). However, this enzyme is mostly found in cancer cells and rarely in normal cells. Thus, cancer cell can possibly immortalized under controlled laboratory conditions.

The Skin Structure

The skin, the largest organ of the body, is divided into dermis and epidermis layers. The outer layer, epidermis, is comprised of epithelial cells while the inner layer, dermis, is mostly fibrous connective tissues (Ekerdt 1090). The epidermal cells protect the skin from external pressures and harmful microorganism penetration. Unlike the epidermis, the dermis is a living tissue. It is composed of nerves, sensory receptors, blood vessels and hair follicle roots. The dermis is further divided into reticular and superficial layers. Around 80% of the dermal tissue is found in reticular layer which is comprised of collagen fibres (Ekerdt 1090). Collagen is a hard protein which binds with water and gives protection to the skin against trauma and dehydration. However, one percent of collagen is perished annually making the skin susceptible to damage. Consequently, the collagen cross-links left behind lessens the elasticity of the skin that leads to wrinkling.

Homeostasis

The life of a cell is largely dependent on the sustainance of internal physiological balance called homeostasis. When homeostasis is disturbed, through the autonomic nervous system, the cell applies responses or measures to restore the balance. In relation to this, age-related changes influence homeostasis. For instance, the inefficacy of nerve conduction or peripheral temperature receptors as well as metabolic rate reduction are natural consequences of aging (Woodrow 25). These phenomena make the individual less sensitive to cold weather and prone to hypothermia.

The Skin at Aging years

As one progresses with age, the function of the skin declines. At young age, the renewal of the epidermis is done every 20th day (Woodrow 30). Beyond the age of 50, the renewal time is increased by one-third as the epidermis is flattened. The layers of the skin then can easily be peeled apart and are prone to pressure sores due to shearing forces. Moreover, the dermal cells are reduced in function and number; fewer skin capillaries are then available for nutrients, oxygen and fluid supply. Nevertheless, the re-epithelization occurs in a 75-year old individual twice as long of that in a 25-year old (Woodrow 31). Thus, at old age, wounds caused by surgery or trauma take a longer healing time. The hormone reduction as age increases lessens the production of sebum that protects skin, nails and hair. In the same way, as the function of the sensory nerves decline, the individual is less sensitive to feel pain, temperature or touch which exposes him or her to the risks of hypothermia, burns, and cuts.

Conclusion

A wide range of environmental and genetic factors affect skin aging. Although the effects of these factors are irreversible, the aging process can possibly be hindered. The aforementioned theories denoted the possible causes of aging as proven by scientific studies. In particular, aging is influenced by several physiological factors which can be aggravated or hindered. Although health and life expectancy are influenced by societal status, the genetic and gender factors of aging are independent from socio-economic conditions. As well, health and life expectancy of every individual are affected by the a range of factors he or she was exposed to throughout his or her life. As such, as the skin is sensitive to enzyme activation induced by the sun’s UV rays, sun exposure then must be minimized to protect the skin. In addition, good skin hygiene and a well-balanced diet are of great help to delay the aging process.

Works Cited

Arking, Robert. The Biology of Aging: Observations and Principles. New York: Oxford University Press, 2006.

Chadwick, Dereck and Goodie, Jamie. “Endocrine Facets of Aging.” Ciba Foundation Symposium. Chichester, West Sussex New York: John Wiley and Sons Ltd., 2002.

Ekerdt, David. “Skin Aging.” Encyclopedia of Aging. New York: Macmillian Reference USA, Gale Group, 2002.

Gewies, Andreas. Introduction to Apoptosis. 2003. Apo Review. 15 April 2009 <http://www.celldeath.de/encyclo/aporev/apointro.pdf>

Hayflict, Leonard. “The Cell Biology of Aging.” Clinical Geriatric Medicine 1 (1985): 15-27.

Macieira-Coelho, Alvaro. Biology of Aging. Berlin: Springer, 2003.

Schulze-Osthoff, Klaus. Apoptosis, Cell Death and Cell Proliferation, 4th ed. Roche Applied Science. Mannheim, Germany: Roche Diagnostics GmbH, 2008

Woodrow, Philip. Ageing: Issues for Physical, Psychological and Social Health. Philadelphia: Whurr Publishing, 2002.

 

Cite this The Biology of Aging

The Biology of Aging. (2017, Feb 08). Retrieved from https://graduateway.com/the-biology-of-aging/

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