<?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>0034-7418</journal-id>
<journal-title><![CDATA[Revista Colombiana de Ciencias Químico - Farmacéuticas]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. colomb. cienc. quim. farm.]]></abbrev-journal-title>
<issn>0034-7418</issn>
<publisher>
<publisher-name><![CDATA[Departamento de Farmácia, Facultad de Ciencias, Universidade Nacional da Colombia]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0034-74182022000100123</article-id>
<article-id pub-id-type="doi">10.15446/rcciquifa.v51n1.102682</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Tempol decreases the levels of reactive oxygen species in human neutrophils and impairs their response to]]></article-title>
<article-title xml:lang="pt"><![CDATA[Tempol diminui os níveis de espécies reativas de oxigênio em neutrófilos humanos e enfraquece a resposta ao Mycobacterium tuberculosis]]></article-title>
<article-title xml:lang="es"><![CDATA[Tempol disminuye los niveles de especies reactivas de oxígeno en neutrófilos humanos y debilita la respuesta hacia Mycobacterium tuberculosis]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Cerdeira]]></surname>
<given-names><![CDATA[Cláudio Daniel]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Chavasco]]></surname>
<given-names><![CDATA[Jorge Kleber]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pereira Lima Brigagão]]></surname>
<given-names><![CDATA[Maísa Ribeiro]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Federal University of Alfenas  ]]></institution>
<addr-line><![CDATA[Minas Gerais MG]]></addr-line>
<country>Brazil</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,University of Alfenas  ]]></institution>
<addr-line><![CDATA[Alfenas MG]]></addr-line>
<country>Brazil</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>51</volume>
<numero>1</numero>
<fpage>123</fpage>
<lpage>151</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S0034-74182022000100123&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S0034-74182022000100123&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S0034-74182022000100123&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[SUMMARY  Background and aims:  Mycobacterium tuberculosis (Mtb), the main causative agent of human tuberculosis (TB), remains as a serious public health problem. The innate immune response following Mtb infection plays a crucial role in preventing the onset of active TB and limiting its spread. Since phagocytes-derived reactive oxygen/nitrogen species (ROS/RNS) during the oxidative burst can fight Mtb, we hypothesized that the use of antioxidants could increase the host's susceptibility to Mtb/TB. In that way, we investigated the effects of the nitroxide Tempol, an antioxidant with superoxide dismutase-like activity, on the response of neutrophils against Mtb.  Methods: Human blood-derived neutrophils were isolated from healthy volunteers and incubated with Mtb (H37Ra) at different multiplicities of infection (MOIs), in the absence or presence of Tempol. The levels of ROS in neutrophils were evaluated using the cytochrome C reduction assay (extracellular O2 &#8226;-) and luminol-(total intracellular and extracellular ROS) and isoluminol-(extracellular ROS) amplified chemiluminescence assay. The killing assay (two-step protocol) checked the mycobactericidal capacity of neutrophils, as calculated the phagocytosis (K  p ) and intracellular killing (Kk) rates.  Results: The levels of ROS and killing capacity in Mtb-stimulated neutrophils were significantly decreased by 450 &#956;M Tempol (p &lt; 0.05). Interestingly, Tempol decreased the k  k of neutrophils, but did not affect their kp, demonstrating that a putative diminution in ROS levels, ultimately, affected the intracellular killing of Mtb.  Conclusion: This study provides insights regarding the role of antioxidants on the neutrophil response toward Mtb, so that our findings deserve to be considered regarding further studies and clinical implications.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN  Contextualización y objetivos:  Mycobacterium tuberculosis (Mtb), el principal agente causal de la tuberculosis humana (TB), es un grave problema de salud pública. La respuesta inmune innata desencadenada en la infección por Mtb juega un papel crucial en la prevención de la aparición de la tuberculosis activa y en la limitación de su propagación. Dado que las especies reactivas de oxígeno/nitrógeno derivadas de los fagocitos (ERO/ERN) durante el burst oxidativo pueden combatir la infección pulmonar por Mtb, planteamos la hipótesis de que el uso de antioxidantes podría aumentar la susceptibilidad del huésped humano hacia Mtb/TB. De esa manera, investigamos los efectos del nitróxido Tempol, un antioxidante con actividad similar a la superóxido dismutasa, sobre la respuesta de los neutrófilos contra Mtb.  Métodos: se aislaron neutrófilos derivados de sangre humana de voluntarios sanos y se incubaron con Mtb (H37Ra) en diferentes multiplicidades de infección (MOI), en ausencia o presencia de Tempol. Los niveles de ERO en neutrófilos se evaluaron mediante el ensayo de la reducción del citocromo C (O2'- extracelular) y el ensayo de quimioluminiscencia, amplificada mediante el uso de luminol (ERO total, intracelular y extracelular) e isoluminol (ERO extracelular). La prueba de actividad microbicida (protocolo de dos pasos) verificó la capacidad micobactericida de los neutrófilos, calculando las tasas de fagocitosis (Kp) y muerte intracelular (Kk).  Resultados: los niveles de ERO y la capacidad micobactericida en neutrófilos estimulados con Mtb disminuyeron significativamente en los grupos tratados con 450 &#956;M de Tempol (p &lt; 0,05). Curiosamente, Tempol disminuyó la tasa de muerte intracelular (Kk) en neutrófilos, pero no tuvo ningún efecto sobre la tasa de fagocitosis (Kp), lo que demuestra que una supuesta disminución en los niveles de ERO, en última instancia, afectó la destrucción intracelular de Mtb.  Conclusión: este estudio proporciona información sobre el papel de los antioxidantes en la respuesta de los neutrófilos hacia Mtb, por lo que nuestros hallazgos merecen ser considerados con respecto a más estudios e implicaciones clínicas.]]></p></abstract>
<abstract abstract-type="short" xml:lang="pt"><p><![CDATA[RESUMO  Contextualização e objetivos:  Mycobacterium tuberculosis (Mtb), principal agente causal da tuberculose humana (TB), é um grave problema de saúde pública. A resposta imune inata desencadeada pela infecção por Mtb desempenha um papel crucial na prevenção do aparecimento da tuberculose ativa e na limitação de sua disseminação. Como as espécies reativas de oxigênio/nitrogênio derivadas de fagó-citos (ERO/ERN) durante a burst oxidativa podem combater a infecção pulmonar por Mtb, hipotetizamos que o uso de antioxidantes poderia aumentar a suscetibilidade do hospedeiro humano ao Mtb/TB. Assim, investigamos os efeitos do nitróxido de Tempol, um antioxidante com atividade semelhante a superóxido dismutase, na resposta de neutrófilos contra o Mtb.  Métodos: neutrófilos derivados de sangue humano foram isolados de voluntários saudáveis e incubados com Mtb(H37Ra) em diferentes multiplicidades de infecção (MOI), na ausência ou presença de Tempol. Os níveis de ERO em neutrófilos foram avaliados por ensaio de depleção de citocromo C (O2&#8226;- extracelular) e ensaio de quimioluminescência, amplificado com luminol (ERO total, intracelular e extracelular) e isoluminol (ERO extracelular). O teste de atividade microbicida (protocolo de duas etapas) verificou a capacidade micobactericida dos neutrófilos, calculando as taxas de fagocitose (Kp) e morte intracelular (Kk).  Resultados: os níveis de ERO e a capacidade micobactericida em neutrófilos estimulados por Mtb diminuíram significativamente nos grupos tratados com Tempol 450 &#956;M (p &lt; 0,05). Curiosamente, Tempol diminuiu a taxa de morte intracelular (Kk) em neutrófilos, mas não teve efeito sobre a taxa de fagocitose (Kp), mostrando que uma diminuição putativa nos níveis de ERO afetou a morte intracelular de Mtb.  Conclusão: este estudo fornece informações sobre o papel dos antioxidantes na resposta dos neutrófilos ao Mtb, portanto, nossos achados merecem consideração para estudos adicionais e implicações clínicas.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Reactive oxygen species]]></kwd>
<kwd lng="en"><![CDATA[antioxidant]]></kwd>
<kwd lng="en"><![CDATA[nitroxide]]></kwd>
<kwd lng="en"><![CDATA[Tempol]]></kwd>
<kwd lng="en"><![CDATA[Mycobacterium tuberculosis]]></kwd>
<kwd lng="en"><![CDATA[tuberculosis]]></kwd>
<kwd lng="es"><![CDATA[Especies reactivas de oxígeno]]></kwd>
<kwd lng="es"><![CDATA[antioxidante]]></kwd>
<kwd lng="es"><![CDATA[nitróxido]]></kwd>
<kwd lng="es"><![CDATA[Tempol]]></kwd>
<kwd lng="es"><![CDATA[Mycobacterium tuberculosis]]></kwd>
<kwd lng="es"><![CDATA[tuberculosis]]></kwd>
<kwd lng="pt"><![CDATA[Espécies reativas de oxigênio]]></kwd>
<kwd lng="pt"><![CDATA[antioxidante]]></kwd>
<kwd lng="pt"><![CDATA[nitróxido]]></kwd>
<kwd lng="pt"><![CDATA[Tempol]]></kwd>
<kwd lng="pt"><![CDATA[Mycobacterium tuberculosis]]></kwd>
<kwd lng="pt"><![CDATA[tuberculose]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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