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    Por favor, use este identificador para citar o enlazar este ítem:http://uvadoc.uva.es/handle/10324/7157

    Título
    Effects of mitochondrial poisons on glutathione redox potential and carotid body chemoreceptor activity
    Autor
    Gómez Niño, María ÁngelesAutoridad UVA Orcid
    Agapito Serrano, María TeresaAutoridad UVA Orcid
    Obeso Cáceres, Ana María de la LuzAutoridad UVA Orcid
    González Martínez, Constancio
    Año del Documento
    2009
    Editorial
    Elsevier
    Descripción
    Producción Científica
    Documento Fuente
    Respiratory Physiology & Neurobiology 165 (2009) 104–111
    Résumé
    Lowoxygen sensing in chemoreceptor cells involves the inhibition of specific plasma membrane K+ channels, suggesting that mitochondria-derived reactive oxygen species (ROS) link hypoxia to K+ channel inhibition, subsequent cell depolarization and activation of neurotransmitter release.We have used several mitochondrial poisons, alone and in combination with the antioxidant N-acetylcysteine (NAC), and quantify their capacity to alter GSH/GSSG levels and glutathione redox potential (EGSH) in rat diaphragm. Selected concentrations of mitochondrial poisons with or without NAC were tested for their capacity to activate neurotransmitter release in chemoreceptor cells and to alter ATP levels in intact rat carotid body (CB).We found that rotenone (1 M), antimycin A (0.2 g/ml) and sodium azide (5mM) decreased EGSH; NAC restored EGSH to control values. At those concentrations mitochondrial poisons activated neurotransmitter release from CB chemoreceptor cells and decreased CB ATP levels, NAC being ineffective to modify these responses. Additional experiments with 3-nitroprionate (5 mM), lower concentrations of rotenone and dinitrophenol revealed variable relationships between EGSH and chemoreceptor cell neurotransmitter release responses and ATP levels. These findings indicate a lack of correlation between mitochondrialgenerated modifications of EGSH and chemoreceptor cells activity. This lack of correlation renders unlikely that alteration of mitochondrial production of ROS is the physiological pathway chemoreceptor cells use to signal hypoxia.
    Materias (normalizadas)
    Neurofisiología
    ISSN
    1569-9048
    Revisión por pares
    Sí
    DOI
    10.1016/j.resp.2008.10.020
    Idioma
    eng
    URI
    http://uvadoc.uva.es/handle/10324/7157
    Derechos
    openAccess
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    • DEP06 - Artículos de revista [352]
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