By Luisa Fernanda Naranjo Pérez. Medicine. UPB-Medellín-Colombia
The DNA is the most important part of the cell, because it has all the information that is fundamental for the maintenance of the cell, the genome and the live; for those reasons is very important to have the check points located phases of the interphase and the beggining of the mitosis. Thanks to this check points, stem cell passed the same information to daughter cells, to mainteing the information complete. When those mechanisms failed, the cell cannot detect the damage and the wrong information, passed through the cells, causing several problems, like cancer, lents opacity and polymorphisms .
The sister chromati exchange (SCEs) is a natural molecular process exchanging genetic material between two identical sister chromatids. Since (SCEs) represent recombinogenic events arising DNA lesions, became a widely used endpoint in the study of mutagenic and clastogenic effects of diferents agents.
In some investigations the studies revealed that S-phase-dependents agents are strong inducers of SCEs, whereas ionizing radiation (IR) and radiomimetic drugs weak inducers of this.
In G2 the majority of DNA double strand breaks (DBSs) are raplidy repaired by NHEJ (non homologous end joinig) in the firs 2-3 hours but a subset of breaks is repaired by HR ( homologous recombination); instead cells damaged by IR remain in G2 for at least 6-8 hours, this is because the IR induced G2 checkpoint provides additional time to repair it.
In this point they found that the homologous recombination, is a minor way to repair the cell, and the majority of the process is done by non homologous end joining. When the irradiated cells were observed in metaphase they observed chromatid type aberrations such gaps and chromatid breaks, that is because they found that the repair of de DNA double strand breaks (DSBs) have some changes in the sister chromatid exchange (SCE), such after the irradiation .
I think that this article open us the door to keep investigating and searching about the cell DNA reparation mechanism and the cell cycle, because this will be the way to found some diseases even before it expressed in the phenotype, specially in cells that are exposed to irradiation.
Many studies, reveal the association between oxidative stress and DNA damage with lens opacities, and in this article specially they refered the damage of the DNA in the lens epithelium, induced by UV light, causing as an effect the development cataract disease.
Polymorphisms of xeroderma pigmentosum complementation group D ( XPD) X-ray complementing group I ( XRCC1) have been very studied Requiered for excision repair of UV damaged DNA. Importan part of nucleotide excision repair (NER) Is involved in single strand breaks, and base excision repair (BER). markers to indicate DNA damage.
In this article they compare this two DNA repair genes between man and woman (studying differents factors, like lifestyles , genetic predisposition, and the exposition to UV light), indicating high risk for females because them mainly present age related cataracts specially the posterior subcapsular type, and with the XPD-312 Asn/Asn gene in common, increasing the risk.
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.
This article is crucial for the medical studies, because it brings us many variables to detect the formation of cataracts and the relation between the two genes treated in the article, how they prevalence or not, by the increasing of damaged DNA in the prevalence of this disease.
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.
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.
In a special way this articles illustrated us how we could relate very common diseases like cancer and cataract, wich epicenter 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.
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 .
MARTINEZ SANCHEZ, Lina María. Biología Molecular. 6ta Edición. UPB Facultad de Medicina. Pp: 81-84 Sister chromatid exchanges occur in G-irradiated cells (January 15, 2011) Polymorphisms in two DNA repair genes (XPD and XRCC1) (Published 12 January 2011)
"Perseverance is not a long race; it is many short races one after another." Walter Elliott