Aging is one of the most hated occurence in our life....

1. REPORT IN CELL BIOLOGY
THE FREE RADICAL THEORY OF AGING
Ronnie Z. Valenciano Jr. BSE 3B
College of Development Education, Central Bicol State University of Agriculture
Introduction
We 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 Formation
Atoms 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.
Radiation
H2O HO· + H· (“·” indicates free radical)
hydroxyl radicals
Free Radical Damage
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.

2. 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·–)
( SOD)
O2·– + O2·– + 2H 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.html
http://images.search.yahoo.com/search/images?p=free+radicals&ei=UTF-8&fr=yfp-t-701&tab=organic&b=113
www.authorstream.com/Presentation/abdulrazzaqM.PHARM-737902-seminar-on-oxygen-free-radicals/

6. http://www.physics.ohio-state.edu/~wilkins/writing/Samples/shortmed/nelson/radicals.html
http://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

7. 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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