By Luisa Fernanda Naranjo Pérez.

Medicine.

UPB-Medellín-Colombia

The DNA is the most important part ofthe cell, because it has all theinformation that is fundamental forthe maintenance of the cell, thegenome and the live; for thosereasons is very important to have thecheck points located phases of theinterphase and the beggining of themitosis.

Thanks to this check points, stem cellpassed the same information todaughter cells, to mainteing theinformation complete. When thosemechanisms failed, the cell cannotdetect the damage and the wronginformation, passed through thecells, causing several problems, likecancer, lents opacity andpolymorphisms .

The sister chromati exchange (SCEs) isa natural molecular processexchanging genetic material betweentwo identical sister chromatids.

Since (SCEs) representrecombinogenic events arising DNA lesions, became a widely usedendpoint in the study of mutagenicand clastogenic effects of diferentsagents.

In some investigations the studiesrevealed that S-phase-dependents agents are stronginducers of SCEs, whereas ionizingradiation (IR) and radiomimeticdrugs weak inducers of this.

In G2 the majority of DNA doublestrand breaks (DBSs) are raplidyrepaired by NHEJ (non homologous endjoinig) in the firs 2-3 hours but a subsetof breaks is repaired by HR (homologous recombination); insteadcells damaged by IR remain in G2 for atleast 6-8 hours, this is because the IRinduced G2 checkpoint providesadditional time to repair it.

In this point they found that thehomologous recombination, is aminor way to repair the cell, andthe majority of the process isdone by non homologous endjoining.

When the irradiated cells were observed inmetaphase they observed chromatid typeaberrations such gaps and chromatid breaks, that isbecause they found that the repair of de DNAdouble strand breaks (DSBs) have some changes inthe sister chromatid exchange (SCE), such after theirradiation .

I think that this article open usthe door to keep investigatingand searching about the cellDNA reparation mechanism

and the cell cycle, because thiswill be the way to found some

diseases even before itexpressed in the

phenotype, specially in cellsthat are exposed to irradiation.

Many studies, reveal the associationbetween oxidative stress and DNA damage with lens opacities, and in this article specially they refered thedamage of the DNA in the lensepithelium, induced by UV light, causing as an effect thedevelopment cataract disease.

Polymorphisms of xeroderma pigmentosumcomplementation group D

(XPD)

X-ray complementing group I (XRCC1)

have been very studied

Requiered for excisionrepair of UV damaged

DNA.Importan part of

nucleotide excisionrepair (NER)

Is involved in single strand breaks, and

base excision repair (BER).

markers to indicate DNA

damage.

In this article they comparethis two DNA repair genesbetween man and woman(studying differentsfactors, like lifestyles , geneticpredisposition, and theexposition to UV light),indicating high risk forfemales because them mainlypresent age related cataractsspecially the posteriorsubcapsular type, and withthe XPD-312 Asn/Asn gene incommon, increasing the risk.

It is suggested that damage to the lensepithelium may result in cataract formationand reported that UV light induced oxidativestress causes the earliest detectable changes inthe epithelial cell redox set point and at theDNA and membrane level damage, in thiscases cataract formation became inevitable.

This article is crucial for the medicalstudies, because it brings us many

variables to detect the formation of cataracts and the relation between thetwo genes treated in the article, how

they prevalence or not, by the increasingof damaged DNA in the prevalence of

this disease.

The reparation mechanism ofDNA, is very important to keepthe genome, and to detectsome irregular things that affectthe patient, and their geneticsgenerations, inducing severalgenetic predisposition of adisease.

The deeply knowledge of Molecular Biology might brings usthe possibilities of treatment for people that suffered diseasesbecause of some cellular anomalies , that are not easy todetect with physically diagnosis, and thanks to this branch ofmedicine we could detect and treat.

In a special way this articles illustrated us how we couldrelate very common diseases like cancer and cataract, wichepicenter of the this sickness were the DNA failed repairmechanism, that expressed it in the development of thedisease and how the DNA knowledge give us a lot of vitalinformation.

The DNA reparation mechanisms, motivate us like futuresdoctors to search the minimal expression of commondiseases, that could let us to search more about the basis ofthe live, DNA. And to continue with the studies and searchesthat could prevent a lot of diseases, just manipulating cells invitro .

MARTINEZ SANCHEZ, Lina María. BiologíaMolecular. 6ta Edición. UPB Facultad de Medicina.Pp: 81-84

Sister chromatid exchanges occur in G-irradiatedcells (January 15, 2011)

Polymorphisms in two DNA repair genes (XPD andXRCC1) (Published 12 January 2011)

"Perseverance is not a long race; it is many short races one after another." Walter Elliott