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<title>Chemoreception in the context of the general biology of ROS</title>
<creator>González Martínez, Constancio</creator>
<creator>Agapito Serrano, María Teresa</creator>
<creator>Rocher Martín, María Asunción</creator>
<creator>Martín González, María del Carmen</creator>
<creator>Vega Agapito, María Victoria</creator>
<creator>Gómez Niño, María Ángeles</creator>
<creator>Rigual Bonastre, Ricardo Jaime</creator>
<creator>Castañeda, Francisco Javier</creator>
<creator>Obeso Cáceres, Ana María de la Luz</creator>
<subject>Respiración celular</subject>
<description>Producción Científica</description>
<description>Superoxide anion is the most important reactive oxygen species (ROS) primarily generated in cells. The main cellular constituents with capabilities&#xd;
to generate superoxide anion areNADPHoxidases and mitochondrial respiratory chain. The emphasis of our article is centered in critically examining&#xd;
hypotheses proposing that ROS generated by NADPH oxidase and mitochondria are key elements in O2-sensing and hypoxic responses generation&#xd;
in carotid body chemoreceptor cells. Available data indicate that chemoreceptor cells express a specific isoform of NADPH oxidase that is activated&#xd;
by hypoxia; generated ROS acting as negative modulators of the carotid body (CB) hypoxic responses. Literature is also consistent in supporting&#xd;
that poisoned respiratory chain can produce high amounts of ROS, making mitochondrial ROS potential triggers-modulators of the CB activation&#xd;
elicited by mitochondrial venoms. However, most data favour the notion that levels of hypoxia, capable of strongly activating chemoreceptor cells,&#xd;
would not increase the rate of ROS production in mitochondria, making mitochondrial ROS unlikely triggers of hypoxic responses in the CB.&#xd;
Finally, we review recent literature on heme oxygenases from two perspectives, as potential O2-sensors in chemoreceptor cells and as generators&#xd;
of bilirubin which is considered to be a ROS scavenger of major quantitative importance in mammalian cells.</description>
<date>2014-11-13</date>
<date>2014-11-13</date>
<date>2007</date>
<type>info:eu-repo/semantics/article</type>
<identifier>Respiratory Physiology &amp; Neurobiology 157 (2007) 30–44</identifier>
<identifier>1569-9048</identifier>
<identifier>http://uvadoc.uva.es/handle/10324/7121</identifier>
<identifier>10.1016/j.resp.2007.01.016</identifier>
<identifier>30</identifier>
<identifier>44</identifier>
<identifier>Respiratory Physiology &amp; Neurobiology</identifier>
<identifier>157</identifier>
<language>eng</language>
<rights>info:eu-repo/semantics/openAccess</rights>
<rights>http://creativecommons.org/licenses/by-nc-nd/4.0/</rights>
<rights>Attribution-NonCommercial-NoDerivatives 4.0 International</rights>
<publisher>Elsevier</publisher>
</thesis></metadata></record></GetRecord></OAI-PMH>