RT info:eu-repo/semantics/article
T1 Effects of mitochondrial poisons on glutathione redox potential and carotid body chemoreceptor activity
A1 Gómez Niño, María Ángeles
A1 Agapito Serrano, María Teresa
A1 Obeso Cáceres, Ana María de la Luz
A1 González, Constancio
K1 Neurofisiología
AB 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+ channelinhibition, subsequent cell depolarization and activation of neurotransmitter release.We have used severalmitochondrial poisons, alone and in combination with the antioxidant N-acetylcysteine (NAC), andquantify 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 toactivate 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 neurotransmitterrelease from CB chemoreceptor cells and decreased CB ATP levels, NAC being ineffective to modifythese responses. Additional experiments with 3-nitroprionate (5 mM), lower concentrations of rotenoneand dinitrophenol revealed variable relationships between EGSH and chemoreceptor cell neurotransmitterrelease responses and ATP levels. These findings indicate a lack of correlation between mitochondrialgeneratedmodifications of EGSH and chemoreceptor cells activity. This lack of correlation renders unlikelythat alteration of mitochondrial production of ROS is the physiological pathway chemoreceptor cells useto signal hypoxia.
PB Elsevier
SN 1569-9048
YR 2009
FD 2009
LK http://uvadoc.uva.es/handle/10324/7157
UL http://uvadoc.uva.es/handle/10324/7157
LA eng
NO Respiratory Physiology & Neurobiology 165 (2009) 104–111
NO Producción Científica
DS UVaDOC
RD 19-nov-2024