<?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>0864-2176</journal-id>
<journal-title><![CDATA[Revista Cubana de Oftalmología]]></journal-title>
<abbrev-journal-title><![CDATA[Rev Cubana Oftalmol]]></abbrev-journal-title>
<issn>0864-2176</issn>
<publisher>
<publisher-name><![CDATA[Editorial Ciencias Médicas]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0864-21762021000200014</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Participación de las especies reactivas de oxígeno en la formación de la catarata]]></article-title>
<article-title xml:lang="en"><![CDATA[Involvement of reactive oxygen species in cataract formation]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Molinet Vega]]></surname>
<given-names><![CDATA[Lázara Mairely]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pérez Pacheco]]></surname>
<given-names><![CDATA[Arturo Iván]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Morell Ochoa]]></surname>
<given-names><![CDATA[Zaylit]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Centro Oftalmológico Hospital General Docente &#8220;Dr. Enrique Cabrera&#8221;  ]]></institution>
<addr-line><![CDATA[ La Habana]]></addr-line>
<country>Cuba</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>06</month>
<year>2021</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>06</month>
<year>2021</year>
</pub-date>
<volume>34</volume>
<numero>2</numero>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_arttext&amp;pid=S0864-21762021000200014&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_abstract&amp;pid=S0864-21762021000200014&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.sld.cu/scielo.php?script=sci_pdf&amp;pid=S0864-21762021000200014&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN La catarata comprende la opacidad del cristalino, la cual puede afectar la corteza y el núcleo subcapsular anterior y posterior de manera progresiva, secundario a la acumulación de proteínas dañadas a este nivel, con pérdida del equilibrio entre la producción y la eliminación de las especies reactivas libres de oxígeno. La importancia de retrasar o identificar marcadores específicos, además de promover un nuevo blanco terapéutico, también es motivo de análisis y de estudio en diferentes líneas de investigación. Se realizó una revisión de la literatura del 01 de enero al 20 de julio del año 2020. Se utilizaron metabuscadores en inglés y español de PUBMED, INFOMED, CLINICALKEY, LILACS, EBSCO, SCIELO, PRISMA y UPTODATE, con el objetivo de identificar la nueva evidencia científica relacionada con el estrés oxidativo y su participación en la formación de la catarata. La barrera del cristalino funciona como un medio de intercambio entre diferentes moléculas, lo que impide el paso de antioxidantes al núcleo y provoca su opacificación. Las mitocondrias a nivel de la corteza del cristalino permiten la remoción de oxígeno. Posteriormente la fosforilación oxidativa forma radicales libres de superóxido que, de manera natural, con el paso del tiempo se acumulan a este nivel. Con la edad, la homeostasis adaptativa pierde la capacidad de responder ante los cambios de estrés oxidativo, por lo que el uso de antioxidantes -de manera profiláctica e intencionada- puede cambiar el destino último para esta patología. La falta de equilibrio en los procesos de óxido-reducción es responsable de la formación de la catarata.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[ABSTRACT Cataract comprises opacification of the crystalline lens, which may progressively affect the cortex and the anterior subcapsular nucleus, secondary to accumulation of damaged proteins on this level, with loss of balance between production and elimination of free reactive oxygen species. The importance of delaying or identifying specific markers, as well as promoting a new therapeutic target, is the object of study and analysis of a variety of research lines. A review was conducted of the literature published from 1 January to 20 July 2020. Use was made of PubMed, Infomed, Clinical Key, Lilacs, EBSCO, SciELO, Prisma and UpToDate metasearch engines in English and Spanish to identify new scientific evidence about oxidative stress and its involvement in cataract formation. The crystalline lens barrier serves as a medium for exchange between various molecules, preventing entrance of antioxidants into the nucleus, which results in opacification. Mitochondria on the crystalline lens cortex allow oxygen removal. Oxidative phosphorylation then forms free superoxide radicals which naturally accumulate on this level with the passing of time. With aging, adaptive homeostasis loses its ability to respond to oxidative stress changes, but the prophylactic, targeted use of antioxidants may change the ultimate fate of this condition. Lack of balance in oxidation-reduction processes is the cause of cataract formation.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Catarata]]></kwd>
<kwd lng="es"><![CDATA[especies reactivas libres de oxígeno]]></kwd>
<kwd lng="es"><![CDATA[proceso de óxido-reducción]]></kwd>
<kwd lng="es"><![CDATA[bioquímica]]></kwd>
<kwd lng="es"><![CDATA[tratamiento]]></kwd>
<kwd lng="en"><![CDATA[Cataract]]></kwd>
<kwd lng="en"><![CDATA[EROS]]></kwd>
<kwd lng="en"><![CDATA[redox]]></kwd>
<kwd lng="en"><![CDATA[biochemistry]]></kwd>
<kwd lng="en"><![CDATA[treatment]]></kwd>
</kwd-group>
</article-meta>
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