REPORT IN CELL BIOLOGYTHE FREE RADICAL THEORY OF AGING

Ronnie Z. Valenciano Jr. BSE 3BCollege of Development Education, Central Bicol State University of Agriculture

IntroductionWe probably think of aging as one of the most hated occurrence in life, especially to the teenagers. Teenagers

are afraid to look too old at their young age. Sometimes they’re blaming the stress cause by hectic class schedule and the overdued projects required by their professors. Meanwhile to lessen up the sagging and drying of their skin, they prefer to walk on the shaded areas and use lotion with high formulation of SPF (Sun Protection Factor). Are teenagers right in doing that defense mechanism to prevent aging? How does aging occur to the human body?

Another intriguing issue about longevity of life span is on the difference on life span of human and animals. Human life expectancy is higher compared to the animals. What would be the reason of this phenomenon? Do their lifestyles affect the span of their life? The answer may dwell on the report about the Free Radical Theory of Aging.

Aging is cause by an atom which has unpaired electrons, making an atom highly reactive. It results to the term Free Radical. Free radical usually attacked mitochondria- the powerhouse of the cell by the process of electron transport chain where oxygen is utilizes to generate energy. To destroy these highly reactive atoms antioxidants are applied to neutralize the unstable atoms.

Discussion of Topics

What is Free Radical?Free radicals are atom or group of atoms with at least one unpaired electron

making it in unstable state, hence making it very reactive. These are organic molecules responsible for ageing, tissue damage and possibly diseases. In the body it is usually an oxygen molecule that has lost electron and will stabilize itself by stealing an electron from a nearby molecule. These are the high energy particles that ricochet wildly and damage cells.

Free Radical FormationAtoms are most stable in the ground state. An atom is considered to be

"ground" when every electron in the outermost shell has a complimentary electron that spins in the opposite direction. If an atom is excited, for example by being exposed to heat, one or more of its electrons may temporarily transferred to an orbital of higher energy, but it will soon return to its ground state.

A free radical is easily formed when a covalent bond between entities is broken and one electron remains with each newly formed atom. Free radicals are highly reactive due to the presence of unpaired electron(s). The most common radical in the biological system is the radical oxygen, which is being referred as reactive oxygen species (ROS). Its production occurs mostly within the mitochondria of the cell. Mitochondria are small membrane-enclosed regions of a cell that produce the chemicals a cell uses for energy. Mitochondria accomplish this task through a mechanism called the "electron transport chain." In this mechanism, electrons are passed between different molecules, with each pass producing useful chemical energy. This is found in the inner mitochondrial membrane, which utilizes oxygen to generate energy in the form of ATP. Oxygen occupies the final position in the electron transport chain. Occasionally, the passed electron incorrectly interacts with oxygen, producing oxygen in radical form, thus chain reaction continues and can be “thousands of events long”.

For example, water can be converted into free radicals when exposed to radiation from the sun.

H2O Radiation HO· + H· (“·” indicates free radical)

Free Radical Damage hydroxyl radicals

The primary site of radical oxygen damage is mitochondrial DNA (mtDNA). Every cell contains an enormous set of molecules called DNA which provide chemical instructions for a cell to function. This DNA is found in the nucleus of the cell, which serves as the "command center" of the cell, as well as in the mitochondria. The cell fixes much of the

damage done to nuclear DNA. However, mitochondrial DNA (mtDNA) cannot be readily fixed. Therefore, extensive mtDNA damage accumulates over time and shuts down mitochondria, causing cells to die and the organism to age.

Protection against Free Radicals

On 1969, Joe McCord and Irwin Fridovich of Duke University discovered an enzyme, superoxide dismutase (SOD). Where function was the destruction of superoxide radical (O2·–)

O2·– + O2·– + 2H ( SOD) H2O2 + O2

If H2O2 becomes free radicals, it is normally destroyed by the enzyme catalase or glutathione peroxidase.

Another way to protect the cell from radicals is by antioxidants. Antioxidants neutralize free radicals, it donate an electron; which make the chain reaction ends.

Recommendation

Unlocking the mystery of aging clarifies the issue about the problem on longevity of the human life expectancy, thus it is recommended to:

1. Make further study on discovering other enzymes against free radicals.2. Enhance natural antioxidants in our body and lessen up intake of dietary supplements.3. Apply this knowledge on further research in development of practical method to prevent and repair free

radical damage

References

Alumaga, Marie Jessica B. et al. Conceptual and Functional Chemistry Modular Approach. Vibal Publishing House: Quezon City,2010.

Molecular and Cell Biology, pp. 35-36.http://www.physics.ohio-state.edu/~wilkins/writing/Samples/shortmed/nelson/radicals.htmlhttp://images.search.yahoo.com/search/images?p=free+radicals&ei=UTF-8&fr=yfp-t-701&tab=organic&b=113www.authorstream.com/Presentation/abdulrazzaqM.PHARM-737902-seminar-on-oxygen-free-radicals/

http://www.physics.ohio-state.edu/~wilkins/writing/Samples/shortmed/nelson/radicals.htmlhttp://images.search.yahoo.com/search/images?p=free+radicals&ei=UTF-8&fr=yfp-t-701&tab=organic&b=113

Abstract. Free radicals are atoms with unpaired electrons. According to the free radical theory, radicals damage cells in an organism, causing aging. Mitochondria, regions of the cell that manufacture chemical energy, produce free radicals and are the primary sites for free radical damage. By eliminating free radicals from cells through genetic means and dietary restriction, laboratories have extended the maximum age of laboratory animals. The administration of antioxidants, which eliminate radicals, to laboratory animals fails to increase maximum lifespan.

The nucleus of an atom is surrounded by a cloud of electrons. These electrons surround the nucleus in pairs, but, occasionally, an atom loses an electron, leaving the atom with an unpaired electron. The atom is then called a "free radical," or sometimes just a "radical," and is very reactive. When cells in the body encounter a radical, the reactive radical may cause destruction in the cell. According to the free radical theory of aging, cells continuously produce free radicals, and constant radical damage eventually kills the cell. When radicals kill or damage enough cells in an organism, the organism ages.1

The production of radical oxygen, the most common radical in biological systems, occurs mostly within the mitochondria of a cell. Mitochondria are small membrane-enclosed regions of a cell that produce the chemicals a cell uses for energy. Mitochondria accomplish this task through a mechanism called the "electron transport chain." In this mechanism, electrons are passed between different molecules, with each pass producing useful chemical energy. Oxygen occupies the final position in the electron transport chain. Occasionally, the passed electron incorrectly interacts with oxygen, producing oxygen in radical form.2

The primary site of radical oxygen damage is mitochondrial DNA (mtDNA). Every cell contains an enormous set of molecules called DNA which provide chemical instructions for a cell to function. This DNA is found in the nucleus of the cell, which serves as the "command center" of the cell, as well as in the mitochondria. The cell fixes much of the damage done to nuclear DNA. However, mitochondrial DNA (mtDNA) cannot be readily fixed. Therefore, extensive mtDNA damage accumulates over time and shuts down mitochondria, causing cells to die and the organism to age.4

Protection of mtDNA from radicals slows aging in laboratory animals. Some laboratories have produced fruit flies that live one-third longer than normal fruit flies. These labs genetically altered the fruit flies to produce more natural antioxidants. Antioxidants are molecules that eliminate radicals, so elevated levels of antioxidants prevent much of the mtDNA damage done by radicals. 3

Other labs severely restricted the food intake of laboratory rats, causing a 50% increase in maximum lifespan compared to rats allowed to eat freely.2 The mitochondria of starved rats are not provided with enough material to function at full capacity. Therefore, the electron transport chains in mitochondria of the starved rats pass fewer electrons. With fewer electrons passed, fewer oxygen radicals are produced, so aging slows.

One main problem with the free radical theory is the failure of antioxidants administered as dietary supplements, like vitamins E and C, to significantly increase maximum lifespan. Proponents of the radical theory believe that dietary antioxidants, unlike natural antioxidants produced by cells, do not reach mitochondrial DNA, leaving this site susceptible to radical attack. Interestingly, even though supplemental antioxidants fail to increase maximum lifespan, they do increase the chances of living to the maximum lifespan. This may be due to antioxidant protection of other parts of the cell, like cellular proteins and membranes, from radical damage.2

The goal of all research on the free radical theory is to slow aging and increase maximum lifespan. The achievements so far are astounding; increasing the lifespan of fruit flies and rats is an impressive feat. Despite such success, no practical applications of the theory have been perfected. Genetic alteration is both controversial and difficult for humans. Starvation, while lengthening lifespan, is an unappealing alternative. Dietary antioxidants fail to increase maximum lifespan. However, the production of radicals and their role in aging is well understood. Further research may apply this knowledge in the development of a practical method to prevent or repair mtDNA radical damage.

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