Uv damage

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Uv damage

  1. 1. DNA Damage Caused by Ultra-VioletRadiationNicolle A. Rosa Mercado, UPR CayeyBIOL. 3095AbstractIn order to decrease the risks of cancer and othergenetic disorders, it is essential for every livingorganism to have a stable DNA. In our world, suchconditions for our DNA molecules would beimpossible due to the fact that uncontrollablefactors, such as ultraviolet (UV) radiation alter theirsequences. This type of electromagnetic radiationcauses lesions in DNA sequences such ascyclobutane pyridine dimers (CPDs) and 6-4photoproducts (6-4 PPs). DNA has several repairmechanisms but these do not always work properlydue to the fact that there might be defects in them aswell. This should be a big concern because DNAlesions might cause deadly disorders. Scientistsshould study ways to keep the DNA sequencesstable in order to prevent genetic disorders.IntroductionDNA is the most important molecule for everyliving organism. In humans, it determines yourphysical appearance and it is believed to be a greatinfluence on your personality. It would be ideal thatsuch an important and complex molecule be keptstable, but it is not so. Many uncontrollable factorscan cause damage in the DNA sequence of differentorganisms. Factors that may affect DNA moleculesinclude environmental factors, smoking, and theDNA replication process itself. The most commonfactor for DNA damage is ultra-violet (UV)radiation.UV RadiationUltra-violet radiation is a type of electromagneticradiation, which means that it may be ejected ortaken in by charged particles. It has a shorterwavelength than that of the visible light. There arethree types of UV radiation: UV-A, being the onefound in black lights, UV-B, being the dangeroustype which we are exposed to because of the sun,and UV-C, which is germicidal and the mostdangerous. They vary according to theirwavelength, UV-A having the greatest and UV-Cthe shortest. UV-B is our biggest concern due to thefact that UV-C is absorbed by the atmosphere and
  2. 2. does not reach us directly from the sun, therefore,not being a threat to our health.Protection from UV radiationWe should protect ourselves from UV exposureby using sun screen and not exposing ourselves toextreme amounts of sunlight. The strongest naturalprotection we have against UV exposure is theozone layer. Due to pollutions, the ozone layer hasbeen slowly breaking over the last decades. Thisdepletion has been mostly provoked by man madechemicals. This has resulted in more UV exposurefor organisms that inhabit the earth. The ozone layeris essential for the survival of terrestrial organisms.It is of extreme importance for humans to find away of slowing or stopping the destruction of theozone layer.DNA Repair MechanismsDNA has many types of repair mechanisms, butthey cannot always detect the mutations due todefects in the repair mechanisms themselves. A verycommon type of DNA repair mechanism isnucleotide excision repair (NER), which correctsdifferent types of damages including thyminedimers provoked by UV radiation. Since we alreadyhave the knowledge of how some of these repairmechanisms work, we should investigate the sourceof what causes them to become damaged and find away to manipulate the conditions of the repairmechanism so it can maintain a stability andprevent several UV induced diseases. In humans,these defects in DNA repair mechanisms result in apredisposition to cancer. The primordial problemwith damage in a human’s DNA sequence is that itmay lead to genetic disorders, such as xerodermapigmentosum, which is a condition that causesextreme sensitivity to light. The most commonresult for human overexposure to UV radiation isskin cancer.DNA damage related proteinsAnother danger presented by overexposure toUV radiation is the fact that a damaged DNAsequence might produce proteins that will not carryout their function appropriately. Proteins that havebeen affected due to UV radiation are referred to asDNA damage related proteins (DDR). UV exposurecan result in the phosphorylation of DDR proteins(Oh et. al 2010). The phosphorylation of proteins
  3. 3. directly affects their function and activity. Sinceproteins play such an important role in every livingorganism, this is very inconvenient.Benefits of UV radiation in some organismsAlthough most of the time it is harmful tohumans, UV exposure might be beneficial to certainspecies. In DNA, some results to UV exposureinclude cyclobutane pyrimidine dimers (CPDs) and6-4 photoproducts (6-4 PPs), which are lesions inthe sequence of the DNA caused by UV radiation.CPDs and 6-4 PPs obstruct DNA transcription andreplication but may be fixed through NER. It hasbeen proven that lesions in the DNA sequence, suchas CPDs and 6-4 PPs, may create resistance tocertain pathogens in plants. It must be taken intoconsideration that plants vary greatly from humansin a variety of ways. In different species of plant,these mutations activate defense mechanisms thatare beneficial to the organism (Kunz et. al 2008). Itwould be interesting to know the exact sites of theselesions in plants and compare its DNA sequence tothat of humans to see how the amino acids in thesequences differ and, from there see if it would bepossible to manipulate the human DNA sequence tobehave similarly.For humans UV has its benefits as well. It isused for treating people with vitiligo, a skindisorder in which the patients lose pigmentation oncertain areas. It is also used to purify drinkingwater. The germicidal properties of UV-C are usedto eliminate microbes as a part of the waterpurification process. UV radiation can be of greathelp when manipulated by humans.CPD retaining basal cellsCPDs and 6-4 PPs may be responsible for theformation of clusters that might lead to skincarcinomas. CPD retaining basal cells are cells thataccumulate CPDs (CRBCs). CRBCs are able toform tumors due to DNA damage, which may leadto the formation of the p53 wild type protein. Thep53 protein is in charge of regulating genes thatprovoke phenomenons, such as apoptosis, withinthe cell. CRBCs are activated by low levels of UVradiation. It has been proven that CRBCs are relatedto the creation of p53 clusters (Nijhofa et. al 2007).UV radiation and cancer
  4. 4. In humans, CPDs and 6-4 PPs may promoteapoptosis provoked by UV exposure in cells thatlack NER (De Lima-Bessa et. al 2007). This is agreat danger because it increases the patientssensitivity to sunlight by making him more prone tocarcinogenesis, which is the beginning of cancerdevelopment. There are three types of cancer causedby UV radiation: basal cell carcinomas, squamouscell carcinomas, and melanoma. Basal andsquamous cells are cells found in the epidermis.Basal cells are those found in the innermost part ofthe epidermis and squamous cells are those found inthe upper part of the epidermis. These two types ofcancers can be stopped easily with the appropriatemethods and are not of such a great threat.Melanoma is the most dangerous type of skincancer and it develops in skin cells known as themelanocytes. After an overexposure of UVradiation, the melanocytes begin to growuncontrollably resulting in cancerous cells. UVradiation is very dangerous due to the fact that theDNA repair mechanisms are able to fix the damagethat this radiation has caused in the DNA sequence.ConclusionsIn conclusion, DNA is the most importantmolecule in every organism and it is highlysusceptible to UV radiation. As the ozone layerbreaks, we become more exposed to UV radiation.There are three types of this electromagneticradiation: UV-A, UV-B, and UV-C. UV-A and UV-B are the only two that are able to reach us. UV-B isthe most dangerous to our DNA sequences.Although DNA has highly specific repairmechanisms, some mutations caused by UV can beignored due to a defect in the repair mechanism.Altered DNA sequences may produce geneticmutations and nonfunctional proteins.Ultra-violet radiation causes DNA damage suchas CDCs and 6-4 PPs that may lead to p53 clusters.This may also result in carcinogenesis. There arethree types of skin cancers, out of which , two areeasily treated, basal cell carcinoma and squamouscell carcinoma. Melanoma is the most dangeroustype of skin cancer. CRDCs might form tumorsleading to p53 clusters. UV radiation presents amayor threat to our health because of its ability todamage DNA sequences. It is our responsibility toprotect ourselves from the harmful UV rays emitted
  5. 5. by sunlight and the most common way to do so isby wearing sunscreen.References:-De Lima-Bessa K, Armelini M, Chigancas V,Jacysin JF, Amarante-Mendes GP, Sarasin A,Menck CFM, (December 2007), CPDs and 6-4PPsplay different roles in UV-induced cell death innormal and NER-deficient human cells, Brazil,DNA Repair, 7:303-312-Hidawi. June 2010. India. September 2010.Availableat:http://www.hindawi.com/journals/jna/2010/592980/-Kunz B, Dando P, Grice D, Mohr P, Schenk P, andCahill D, (October 2008), UV-Induced DNADamage Promotes Resistance to the BiotrophicPathogen Hyaloperonospora parasitica inArabidopsis, Rockville, United States, AmericanSociety of Plant Biologists,148:1021-103-Moné M, Volker M, Nikaido O, Mullenders L, vanZeeland A, Vershure PJ, Manders E, van Driel R,(September 2001), Local UV-induced DNA damagein cell nuclei results in local transcription inhibition,Amsterdam, EMBO Reports, 21:1013-1017-Nijhofa J, Muldera, Aat M, Speksnijderb, EwoudN, Hoogervorstb, Esther M, Mullendersc, Leon H,De Gruijl M, Frank R, (July 2007), Growthstimulation of UV-induced DNA damage retainingepidermal basal cells gives rise to clusters of p53overexpressing cells, The Netherlands, DNA Repair6:1642-1650-Oh K, Bustin M, Mazur S, Appellac E, Kraemer K,(September 2010), UV-induced histone H2AXphosphorylation and DNA damage related proteinsaccumulate and persist in nucleotide excisionrepair-deficient XP-B cells, United States, DNARepair, 10:5-15.-Scitable. 2008. Nature Education. 2008. Availableat: http://www.nature.com/scitable/topicpage/dna-damage-repair-mechanisms-for-maintaining-dna-344
  6. 6. by sunlight and the most common way to do so isby wearing sunscreen.References:-De Lima-Bessa K, Armelini M, Chigancas V,Jacysin JF, Amarante-Mendes GP, Sarasin A,Menck CFM, (December 2007), CPDs and 6-4PPsplay different roles in UV-induced cell death innormal and NER-deficient human cells, Brazil,DNA Repair, 7:303-312-Hidawi. June 2010. India. September 2010.Availableat:http://www.hindawi.com/journals/jna/2010/592980/-Kunz B, Dando P, Grice D, Mohr P, Schenk P, andCahill D, (October 2008), UV-Induced DNADamage Promotes Resistance to the BiotrophicPathogen Hyaloperonospora parasitica inArabidopsis, Rockville, United States, AmericanSociety of Plant Biologists,148:1021-103-Moné M, Volker M, Nikaido O, Mullenders L, vanZeeland A, Vershure PJ, Manders E, van Driel R,(September 2001), Local UV-induced DNA damagein cell nuclei results in local transcription inhibition,Amsterdam, EMBO Reports, 21:1013-1017-Nijhofa J, Muldera, Aat M, Speksnijderb, EwoudN, Hoogervorstb, Esther M, Mullendersc, Leon H,De Gruijl M, Frank R, (July 2007), Growthstimulation of UV-induced DNA damage retainingepidermal basal cells gives rise to clusters of p53overexpressing cells, The Netherlands, DNA Repair6:1642-1650-Oh K, Bustin M, Mazur S, Appellac E, Kraemer K,(September 2010), UV-induced histone H2AXphosphorylation and DNA damage related proteinsaccumulate and persist in nucleotide excisionrepair-deficient XP-B cells, United States, DNARepair, 10:5-15.-Scitable. 2008. Nature Education. 2008. Availableat: http://www.nature.com/scitable/topicpage/dna-damage-repair-mechanisms-for-maintaining-dna-344

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