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<dc:title>Significance of ROS in oxygen sensing in cell systems with sensitivy to ohysiological hypoxia</dc:title>
<dc:creator>González Martínez, Constancio</dc:creator>
<dc:creator>Sanz Alfayate, Gloria</dc:creator>
<dc:creator>Agapito Serrano, María Teresa</dc:creator>
<dc:creator>Gómez Niño, María Ángeles</dc:creator>
<dc:creator>Rocher Martín, María Asunción</dc:creator>
<dc:creator>Obeso Cáceres, Ana María de la Luz</dc:creator>
<dc:subject>Neurofisiología</dc:subject>
<dc:description>Reactive oxygen species (ROS) are oxygen-containing molecular entities which are more potent and effective&#xd;
oxidizing agents than is molecular oxygen itself. With the exception of phagocytic cells, where ROS play an important&#xd;
physiological role in defense reactions, ROS have classically been considered undesirable byproducts of cell&#xd;
metabolism, existing several cellular mechanisms aimed to dispose them. Recently, however, ROS have been&#xd;
considered important intracellular signaling molecules, which may act as mediators or second messengers in many cell&#xd;
functions. This is the proposed role for ROS in oxygen sensing in systems, such as carotid body chemoreceptor cells,&#xd;
pulmonary artery smooth muscle cells, and erythropoietin-producing cells. These unique cells comprise essential parts&#xd;
of homeostatic loops directed to maintain oxygen levels in multicellular organisms in situations of hypoxia. The&#xd;
present article examines the possible significance of ROS in these three cell systems, and proposes a set of criteria that&#xd;
ROS should satisfy for their consideration as mediators in hypoxic transduction cascades. In none of the three cell&#xd;
types do ROS satisfy these criteria, and thus it appears that alternative mechanisms are responsible for the&#xd;
transduction cascades linking hypoxia to the release of neurotransmitters in chemoreceptor cells, contraction in&#xd;
pulmonary artery smooth muscle cells and erythropoietin secretion in erythropoietin producing cells.</dc:description>
<dc:date>2014-11-17T08:45:18Z</dc:date>
<dc:date>2014-11-17T08:45:18Z</dc:date>
<dc:date>2002</dc:date>
<dc:type>info:eu-repo/semantics/article</dc:type>
<dc:identifier>Respiratory Physiology &amp; Neurobiology 132 (2002) 17–41</dc:identifier>
<dc:identifier>1569-9048</dc:identifier>
<dc:identifier>http://uvadoc.uva.es/handle/10324/7168</dc:identifier>
<dc:identifier>10.1016/S1569-9048(02)00047-2</dc:identifier>
<dc:identifier>17</dc:identifier>
<dc:identifier>41</dc:identifier>
<dc:identifier>Respiratory Physiology &amp; Neurobiology</dc:identifier>
<dc:identifier>132</dc:identifier>
<dc:language>eng</dc:language>
<dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
<dc:rights>http://creativecommons.org/licenses/by-nc-nd/4.0/</dc:rights>
<dc:rights>Attribution-NonCommercial-NoDerivatives 4.0 International</dc:rights>
<dc:publisher>Elsevier</dc:publisher>
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