1. By Luisa Fernanda Naranjo Pérez. Medicine. UPB-Medellín-Colombia Sister chromatid exchanges occur in G2-irradiated cellsAND Polymorphisms in two DNA repair genes (XPD and XRCC1) –association with age related cataracts
4. INTRODUCTION The DNA isthemostimportantpart of thecell, becauseit has alltheinformationthatis fundamental forthemaintenance of thecell, thegenome and thelive;forthosereasonsisveryimportanttohavethecheckpointslocatedphases of theinterphase and thebeggining of the mitosis. Thankstothischeckpoints, stemcellpassedthesameinformationtodaughtercells, tomainteingtheinformation complete. Whenthosemechanismsfailed, thecellcannotdetectthedamage and thewronginformation, passedthroughthecells, causingseveralproblems, likecancer, lentsopacity and polymorphisms.
6. Sister chromatid exchanges occur in G2-irradiated cells Thesisterchromatiexchange (SCEs) is a natural molecular processexchanginggenetic material betweentwoidenticalsisterchromatids. Since (SCEs) representrecombinogeniceventsarising DNA lesions, became a widelyusedendpoint in thestudy of mutagenic and clastogeniceffects of diferentsagents.
7. Sister chromatid exchanges occur in G2-irradiated cells In someinvestigationsthestudiesrevealedthat S-phase-dependentsagents are stronginducers of SCEs, whereasionizingradiation (IR) and radiomimeticdrugsweakinducers of this.
8. Sister chromatid exchanges occur in G2-irradiated cells In G2 themajority of DNA doublestrandbreaks (DBSs) are raplidyrepairedby NHEJ (non homologousendjoinig) in thefirs 2-3 hoursbut a subset of breaksisrepairedby HR ( homologousrecombination); insteadcellsdamagedby IR remain in G2 for at least 6-8 hours, thisisbecausethe IR induced G2 checkpointprovidesadditional time torepairit.
9. Sister chromatid exchanges occur in G2-irradiated cells Whentheirradiatedcellswereobserved in metaphasetheyobservedchromatidtypeaberrationssuch gaps and chromatidbreaks, thatisbecausetheyfoundthattherepair of de DNA doublestrandbreaks (DSBs) havesomechanges in thesisterchromatidexchange (SCE), suchaftertheirradiation . In this point they found that thehomologous recombination, is a minor way to repair the cell, and the majority of the process is done by non homologous end joining.
10. OBSERVATION I thinkthatthisarticle open usthedoortokeepinvestigating and searchingaboutthecell DNA reparationmechanism and thecellcycle, becausethiswillbethewaytofoundsomediseasesevenbeforeitexpressed in thephenotype, specially in cellsthat are exposedtoirradiation.
11. Polymorphisms in two DNA repair genes (XPD and XRCC1) – association with age related cataracts
12. Polymorphisms in two DNA repair genes (XPD and XRCC1) –association with age related cataracts Manystudies, revealtheassociationbetweenoxidative stress and DNA damagewithlensopacities, and in thisarticlespeciallytheyreferedthedamage of the DNA in thelensepithelium, inducedby UV light, causing as aneffectthedevelopmentcataractdisease.
13. Polymorphisms in two DNA repair genes (XPD and XRCC1) –association with age related cataracts Polymorphisms of xerodermapigmentosumcomplementationgroup D (XPD) X-ray complementing group I (XRCC1) Is involved in single strand breaks, and base excision repair (BER). have been very studied Requieredforexcisionrepair of UV damaged DNA. Importan part of nucleotideexcisionrepair (NER) markers to indicate DNA damage.
14. Polymorphisms in two DNA repair genes (XPD and XRCC1) –association with age related cataracts In thisarticlethey compare thistwo DNA repair genes betweenman and woman (studyingdifferentsfactors, likelifestyles , geneticpredisposition, and theexpositionto UV light), indicatinghighriskforfemalesbecausethemmainlypresentagerelatedcataractsspeciallythe posterior subcapsulartype, and withthe XPD-312 Asn/Asn gene in common, increasingtherisk.
15. Polymorphisms in two DNA repair genes (XPD and XRCC1) –association with age related cataracts It is suggested that damage to the lens epithelium may result in cataract formation and reported that UV light induced oxidative stress causes the earliest detectable changes in the epithelial cell redox set point and at the DNA and membrane level damage, in this cases cataract formation became inevitable.
16. OBSERVATION Thisarticleis crucial forthemedicalstudies, becauseitbringsusmany variables todetecttheformation of cataracts and therelationbetweenthetwo genes treated in thearticle, howtheyprevalenceornot, bytheincreasing of damaged DNA in theprevalence of thisdisease.
17. MEDICAL UTILITY The reparation mechanism of DNA, is very important to keep the genome, and to detect some irregular things that affect the patient, and their genetics generations, inducing several genetic predisposition of a disease.
18. MEDICALUTILITY The deeply knowledge of Molecular Biology might brings us the possibilities of treatment for people that suffered diseases because of some cellular anomalies , that are not easy to detect with physically diagnosis, and thanks to this branch of medicine we could detect and treat.
19. MEDICALUTILITY In a special way this articles illustrated us how we could relate very common diseases like cancer and cataract, wichepicenter of the this sickness were the DNA failed repair mechanism, that expressed it in the development of the disease and how the DNA knowledge give us a lot of vital information.
20. MEDICALUTILITY The DNA reparation mechanisms, motivate us like futures doctors to search the minimal expression of common diseases, that could let us to search more about the basis of the live, DNA. And to continue with the studies and searches that could prevent a lot of diseases, just manipulating cells in vitro .
21. BIBLIOGRAPHY MARTINEZ SANCHEZ, Lina María. Biología Molecular. 6ta Edición. UPB Facultad de Medicina. Pp: 81-84 Sisterchromatidexchangesoccur in G-irradiatedcells(January15, 2011) Polymorphisms in two DNA repair genes (XPD and XRCC1) (Published 12 January 2011)
22. THANK YOU!!! "Perseverance is not a long race; it is many short races one after another." Walter Elliott
