<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>1816-8949</journal-id>
<journal-title><![CDATA[Anales de la Facultad de Ciencias Médicas (Asunción)]]></journal-title>
<abbrev-journal-title><![CDATA[An. Fac. Cienc. Méd. (Asunción)]]></abbrev-journal-title>
<issn>1816-8949</issn>
<publisher>
<publisher-name><![CDATA[EFACIM. Editorial de la Facultad de Ciencias Médicas - Universidad Nacional de Asunción]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1816-89492022000100027</article-id>
<article-id pub-id-type="doi">10.18004/anales/2022.055.01.27</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Ensayo del cometa como bioindicador de inestabilidad genómica en pacientes diabéticos hemodializados]]></article-title>
<article-title xml:lang="en"><![CDATA[Comet assay as a bioindicator of genomic instability in hemodialysis diabetic patients]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Franco de Diana]]></surname>
<given-names><![CDATA[Deidamia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Segovia]]></surname>
<given-names><![CDATA[Jaime]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Cabrera]]></surname>
<given-names><![CDATA[Walter]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Castiglioni]]></surname>
<given-names><![CDATA[Diana]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[López]]></surname>
<given-names><![CDATA[Nery]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Urdapilleta]]></surname>
<given-names><![CDATA[Natalia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Schupp]]></surname>
<given-names><![CDATA[Miriam]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Dure]]></surname>
<given-names><![CDATA[Juan]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Santa-Cruz]]></surname>
<given-names><![CDATA[Francisco]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Católica &#8220;Nuestra Señora de la Asunción&#8221; Facultad de Ciencias de la Salud Laboratorio de Genética Toxicológica]]></institution>
<addr-line><![CDATA[Asunción ]]></addr-line>
<country>Paraguay</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad Católica &#8220;Nuestra Señora de la Asunción&#8221; Facultad de Ciencias de la Salud Cátedra de Fisiopatología]]></institution>
<addr-line><![CDATA[Asunción ]]></addr-line>
<country>Paraguay</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>04</month>
<year>2022</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>04</month>
<year>2022</year>
</pub-date>
<volume>55</volume>
<numero>1</numero>
<fpage>27</fpage>
<lpage>38</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.iics.una.py/scielo.php?script=sci_arttext&amp;pid=S1816-89492022000100027&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.iics.una.py/scielo.php?script=sci_abstract&amp;pid=S1816-89492022000100027&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.iics.una.py/scielo.php?script=sci_pdf&amp;pid=S1816-89492022000100027&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN  Introducción:  Procesos como la mutagénesis, la carcinogénesis y la teratogénesis son producto de la interacción de agentes de origen endógeno como exógeno que interactúan con la molécula de ADN en forma crónica produciendo rupturas en la doble hélice, y en cromosomas completos resultando en la inestabilidad genómica. El estrés oxidativo al que se encuentran sometidas las células al formarse las especies reactivas de oxígeno (ROS) y también las especies reactivas de nitrógeno (RNS), que pueden provenir de radicales producidos a consecuencia de la diabetes o en estados iniciales de la enfermedad renal crónica o como respuesta a procesos inflamatorios en estados avanzados de estas patologías, actúan como agentes genotóxicos endógenos.  Objetivos:  Esta investigación tuvo como objetivo determinar el daño basal en la molécula de ADN de pacientes diabéticos hemodializados, a través del ensayo del Cometa, como un bioindicador de inestabilidad genómica., durante seis meses de tratamiento.  Materiales y métodos:  Se planteó un estudio longitudinal prospectivo de cohorte para comparar los diferentes niveles de daño antes y durante los primeros seis del tratamiento de hemodiálisis. Se evaluó con el test del cometa o electroforesis de células individuales, el daño basal en muestras de sangre venosa de pacientes diagnosticados con Diabetes de tipo II como control negativo y en pacientes diabéticos con enfermedad renal crónica antes de iniciar el tratamiento de diálisis y luego durante el tratamiento. Se utilizó el test de t- Student para muestras independientes y emparejadas.  Resultados:  Se observó un aumento significativo de daño basal y oxidativo en el material genético de pacientes diabéticos con enfermedad renal crónica, comparados con los controles negativos (p&lt; 0.005) y se observó, además, que el daño celular aumenta con el tratamiento de hemodiálisis (p&lt;0.005).  Conclusión:  Los resultados obtenidos en esta investigación permiten concluir que el estrés oxidativo tiene un efecto genotóxico y que el nivel de daño genético es un buen bioindicador del avance de la enfermedad renal crónica y que la hemodiálisis induce a un aumento de daño a nivel del material genético, aumentando el riesgo de carcinogénesis.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[ABSTRACT  Introduction:  Processes such as mutagenesis, carcinogenesis and teratogenesis are the product of the interaction of agents of endogenous and exogenous origin that interact with the DNA molecule in a chronic way producing ruptures in the double helix, and in complete chromosomes resulting in genomic instability. The oxidative stress to which the cells are subjected when reactive oxygen species (ROS) and reactive nitrogen species (RNS) are formed, which may come from radicals produced as a result of diabetes or in initial stages of chronic kidney disease or in response to inflammatory processes in advanced stages of these pathologies, act as endogenous genotoxic agents.  Objectives:  This research aimed to determine the basal damage in the DNA molecule of hemodialyzed diabetic patients, through the Comet assay, as a bioindicator of genomic instability, during six months of treatment.  Materials and methods:  For this research, a prospective longitudinal cohort study was proposed to compare the different levels of genetic damage before and during the first six of hemodialysis treatment. Baseline damage was evaluated with the comet test or single cell electrophoresis, in venous blood samples from patients diagnosed with Type II Diabetes as a negative control and in diabetic patients with chronic kidney disease before starting dialysis treatment and then during treatment.  Results:  A significant increase in basal and oxidative damage was observed in the genetic material of diabetic patients with chronic kidney disease, compared to negative controls (p&lt; 0.005) and it was also observed that cell damage increases with hemodialysis treatment (p&lt;0.005). The t-Student test was used for independent and paired samples.  Conclusion:  The results obtained in this research allow us to conclude that oxidative stress has a genotoxic effect and that the level of genetic damage is a good bioindicator of the progression of chronic kidney disease and that hemodialysis induces an increase in damage at the level of the genetic material, increasing the risk of carcinogenesis.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Ensayo del cometa]]></kwd>
<kwd lng="es"><![CDATA[Hemodiálisis]]></kwd>
<kwd lng="es"><![CDATA[Inestabilidad genómica]]></kwd>
<kwd lng="es"><![CDATA[Daño oxidativo del ADN.]]></kwd>
<kwd lng="en"><![CDATA[Comet assay]]></kwd>
<kwd lng="en"><![CDATA[Hemodialysis]]></kwd>
<kwd lng="en"><![CDATA[Genomic instability]]></kwd>
<kwd lng="en"><![CDATA[Oxidative DNA damage.]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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