1. DNA Damage Caused by Ultra-Violet
Radiation
Nicolle A. Rosa Mercado, UPR Cayey
BIOL. 3095
Abstract
In order to decrease the risks of cancer and other
genetic disorders, it is essential for every living
organism to have a stable DNA. In our world, such
conditions for our DNA molecules would be
impossible due to the fact that uncontrollable
factors, such as ultraviolet (UV) radiation alter their
sequences. This type of electromagnetic radiation
causes lesions in DNA sequences such as
cyclobutane pyridine dimers (CPDs) and 6-4
photoproducts (6-4 PPs). DNA has several repair
mechanisms but these do not always work properly
due to the fact that there might be defects in them as
well. This should be a big concern because DNA
lesions might cause deadly disorders. Scientists
should study ways to keep the DNA sequences
stable in order to prevent genetic disorders.
Introduction
DNA is the most important molecule for every
living organism. In humans, it determines your
physical appearance and it is believed to be a great
influence on your personality. It would be ideal that
such an important and complex molecule be kept
stable, but it is not so. Many uncontrollable factors
can cause damage in the DNA sequence of different
organisms. Factors that may affect DNA molecules
include environmental factors, smoking, and the
DNA replication process itself. The most common
factor for DNA damage is ultra-violet (UV)
radiation.
UV Radiation
Ultra-violet radiation is a type of electromagnetic
radiation, which means that it may be ejected or
taken in by charged particles. It has a shorter
wavelength than that of the visible light. There are
three types of UV radiation: UV-A, being the one
found in black lights, UV-B, being the dangerous
type which we are exposed to because of the sun,
and UV-C, which is germicidal and the most
dangerous. They vary according to their
wavelength, UV-A having the greatest and UV-C
the shortest. UV-B is our biggest concern due to the
fact that UV-C is absorbed by the atmosphere and

2. does not reach us directly from the sun, therefore,
not being a threat to our health.
Protection from UV radiation
We should protect ourselves from UV exposure
by using sun screen and not exposing ourselves to
extreme amounts of sunlight. The strongest natural
protection we have against UV exposure is the
ozone layer. Due to pollutions, the ozone layer has
been slowly breaking over the last decades. This
depletion has been mostly provoked by man made
chemicals. This has resulted in more UV exposure
for organisms that inhabit the earth. The ozone layer
is essential for the survival of terrestrial organisms.
It is of extreme importance for humans to find a
way of slowing or stopping the destruction of the
ozone layer.
DNA Repair Mechanisms
DNA has many types of repair mechanisms, but
they cannot always detect the mutations due to
defects in the repair mechanisms themselves. A very
common type of DNA repair mechanism is
nucleotide excision repair (NER), which corrects
different types of damages including thymine
dimers provoked by UV radiation. Since we already
have the knowledge of how some of these repair
mechanisms work, we should investigate the source
of what causes them to become damaged and find a
way to manipulate the conditions of the repair
mechanism so it can maintain a stability and
prevent several UV induced diseases. In humans,
these defects in DNA repair mechanisms result in a
predisposition to cancer. The primordial problem
with damage in a human’s DNA sequence is that it
may lead to genetic disorders, such as xeroderma
pigmentosum, which is a condition that causes
extreme sensitivity to light. The most common
result for human overexposure to UV radiation is
skin cancer.
DNA damage related proteins
Another danger presented by overexposure to
UV radiation is the fact that a damaged DNA
sequence might produce proteins that will not carry
out their function appropriately. Proteins that have
been affected due to UV radiation are referred to as
DNA damage related proteins (DDR). UV exposure
can result in the phosphorylation of DDR proteins
(Oh et. al 2010). The phosphorylation of proteins

3. directly affects their function and activity. Since
proteins play such an important role in every living
organism, this is very inconvenient.
Benefits of UV radiation in some organisms
Although most of the time it is harmful to
humans, UV exposure might be beneficial to certain
species. In DNA, some results to UV exposure
include cyclobutane pyrimidine dimers (CPDs) and
6-4 photoproducts (6-4 PPs), which are lesions in
the sequence of the DNA caused by UV radiation.
CPDs and 6-4 PPs obstruct DNA transcription and
replication but may be fixed through NER. It has
been proven that lesions in the DNA sequence, such
as CPDs and 6-4 PPs, may create resistance to
certain pathogens in plants. It must be taken into
consideration that plants vary greatly from humans
in a variety of ways. In different species of plant,
these mutations activate defense mechanisms that
are beneficial to the organism (Kunz et. al 2008). It
would be interesting to know the exact sites of these
lesions in plants and compare its DNA sequence to
that of humans to see how the amino acids in the
sequences differ and, from there see if it would be
possible to manipulate the human DNA sequence to
behave similarly.
For humans UV has its benefits as well. It is
used for treating people with vitiligo, a skin
disorder in which the patients lose pigmentation on
certain areas. It is also used to purify drinking
water. The germicidal properties of UV-C are used
to eliminate microbes as a part of the water
purification process. UV radiation can be of great
help when manipulated by humans.
CPD retaining basal cells
CPDs and 6-4 PPs may be responsible for the
formation of clusters that might lead to skin
carcinomas. CPD retaining basal cells are cells that
accumulate CPDs (CRBCs). CRBCs are able to
form tumors due to DNA damage, which may lead
to the formation of the p53 wild type protein. The
p53 protein is in charge of regulating genes that
provoke phenomenons, such as apoptosis, within
the cell. CRBCs are activated by low levels of UV
radiation. It has been proven that CRBCs are related
to the creation of p53 clusters (Nijhofa et. al 2007).
UV radiation and cancer

4. In humans, CPDs and 6-4 PPs may promote
apoptosis provoked by UV exposure in cells that
lack NER (De Lima-Bessa et. al 2007). This is a
great danger because it increases the patients
sensitivity to sunlight by making him more prone to
carcinogenesis, which is the beginning of cancer
development. There are three types of cancer caused
by UV radiation: basal cell carcinomas, squamous
cell carcinomas, and melanoma. Basal and
squamous cells are cells found in the epidermis.
Basal cells are those found in the innermost part of
the epidermis and squamous cells are those found in
the upper part of the epidermis. These two types of
cancers can be stopped easily with the appropriate
methods and are not of such a great threat.
Melanoma is the most dangerous type of skin
cancer and it develops in skin cells known as the
melanocytes. After an overexposure of UV
radiation, the melanocytes begin to grow
uncontrollably resulting in cancerous cells. UV
radiation is very dangerous due to the fact that the
DNA repair mechanisms are able to fix the damage
that this radiation has caused in the DNA sequence.
Conclusions
In conclusion, DNA is the most important
molecule in every organism and it is highly
susceptible to UV radiation. As the ozone layer
breaks, we become more exposed to UV radiation.
There are three types of this electromagnetic
radiation: UV-A, UV-B, and UV-C. UV-A and UV-
B are the only two that are able to reach us. UV-B is
the most dangerous to our DNA sequences.
Although DNA has highly specific repair
mechanisms, some mutations caused by UV can be
ignored due to a defect in the repair mechanism.
Altered DNA sequences may produce genetic
mutations and nonfunctional proteins.
Ultra-violet radiation causes DNA damage such
as CDCs and 6-4 PPs that may lead to p53 clusters.
This may also result in carcinogenesis. There are
three types of skin cancers, out of which , two are
easily treated, basal cell carcinoma and squamous
cell carcinoma. Melanoma is the most dangerous
type of skin cancer. CRDCs might form tumors
leading to p53 clusters. UV radiation presents a
mayor threat to our health because of its ability to
damage DNA sequences. It is our responsibility to
protect ourselves from the harmful UV rays emitted

5. by sunlight and the most common way to do so is
by wearing sunscreen.
References:
-De Lima-Bessa K, Armelini M, Chigancas V,
Jacysin JF, Amarante-Mendes GP, Sarasin A,
Menck CFM, (December 2007), CPDs and 6-4PPs
play different roles in UV-induced cell death in
normal and NER-deficient human cells, Brazil,
DNA Repair, 7:303-312
-Hidawi. June 2010. India. September 2010.
Available
at:http://www.hindawi.com/journals/jna/2010/5929
80/
-Kunz B, Dando P, Grice D, Mohr P, Schenk P, and
Cahill D, (October 2008), UV-Induced DNA
Damage Promotes Resistance to the Biotrophic
Pathogen Hyaloperonospora parasitica in
Arabidopsis, Rockville, United States, American
Society of Plant Biologists,148:1021-103
-Moné M, Volker M, Nikaido O, Mullenders L, van
Zeeland A, Vershure PJ, Manders E, van Driel R,
(September 2001), Local UV-induced DNA damage
in cell nuclei results in local transcription inhibition,
Amsterdam, EMBO Reports, 21:1013-1017
-Nijhofa J, Muldera, Aat M, Speksnijderb, Ewoud
N, Hoogervorstb, Esther M, Mullendersc, Leon H,
De Gruijl M, Frank R, (July 2007), Growth
stimulation of UV-induced DNA damage retaining
epidermal basal cells gives rise to clusters of p53
overexpressing cells, The Netherlands, DNA Repair
6:1642-1650
-Oh K, Bustin M, Mazur S, Appellac E, Kraemer K,
(September 2010), UV-induced histone H2AX
phosphorylation and DNA damage related proteins
accumulate and persist in nucleotide excision
repair-deficient XP-B cells, United States, DNA
Repair, 10:5-15.
-Scitable. 2008. Nature Education. 2008. Available
at: http://www.nature.com/scitable/topicpage/dna-
damage-repair-mechanisms-for-maintaining-dna-
344

6. by sunlight and the most common way to do so is
by wearing sunscreen.
References:
-De Lima-Bessa K, Armelini M, Chigancas V,
Jacysin JF, Amarante-Mendes GP, Sarasin A,
Menck CFM, (December 2007), CPDs and 6-4PPs
play different roles in UV-induced cell death in
normal and NER-deficient human cells, Brazil,
DNA Repair, 7:303-312
-Hidawi. June 2010. India. September 2010.
Available
at:http://www.hindawi.com/journals/jna/2010/5929
80/
-Kunz B, Dando P, Grice D, Mohr P, Schenk P, and
Cahill D, (October 2008), UV-Induced DNA
Damage Promotes Resistance to the Biotrophic
Pathogen Hyaloperonospora parasitica in
Arabidopsis, Rockville, United States, American
Society of Plant Biologists,148:1021-103
-Moné M, Volker M, Nikaido O, Mullenders L, van
Zeeland A, Vershure PJ, Manders E, van Driel R,
(September 2001), Local UV-induced DNA damage
in cell nuclei results in local transcription inhibition,
Amsterdam, EMBO Reports, 21:1013-1017
-Nijhofa J, Muldera, Aat M, Speksnijderb, Ewoud
N, Hoogervorstb, Esther M, Mullendersc, Leon H,
De Gruijl M, Frank R, (July 2007), Growth
stimulation of UV-induced DNA damage retaining
epidermal basal cells gives rise to clusters of p53
overexpressing cells, The Netherlands, DNA Repair
6:1642-1650
-Oh K, Bustin M, Mazur S, Appellac E, Kraemer K,
(September 2010), UV-induced histone H2AX
phosphorylation and DNA damage related proteins
accumulate and persist in nucleotide excision
repair-deficient XP-B cells, United States, DNA
Repair, 10:5-15.
-Scitable. 2008. Nature Education. 2008. Available
at: http://www.nature.com/scitable/topicpage/dna-
damage-repair-mechanisms-for-maintaining-dna-
344