2024-03-28T16:47:52Zhttp://uvadoc.uva.es/oai/requestoai:uvadoc.uva.es:10324/71572021-06-23T09:51:25Zcom_10324_1134com_10324_931com_10324_894col_10324_1213
2014-11-14T12:13:32Z
urn:hdl:10324/7157
Effects of mitochondrial poisons on glutathione redox potential and carotid body chemoreceptor activity
Gómez Niño, María Ángeles
Agapito Serrano, María Teresa
Obeso Cáceres, Ana María de la Luz
González, Constancio
Neurofisiología
Producción Científica
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.
2014-11-14T12:13:32Z
2014-11-14T12:13:32Z
2009
info:eu-repo/semantics/article
Respiratory Physiology & Neurobiology 165 (2009) 104–111
1569-9048
http://uvadoc.uva.es/handle/10324/7157
10.1016/j.resp.2008.10.020
104
111
Respiratory Physiology & Neurobiology
165
eng
info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-nd/4.0/
Attribution-NonCommercial-NoDerivatives 4.0 International
Elsevier