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Redox properties of the adenoside triphosphate‐sensitive K + channel in brain mitochondria
Author(s) -
Fornazari Maynara,
de Paula Juliana G.,
Castilho Roger F.,
Kowaltowski Alicia J.
Publication year - 2008
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.21614
Subject(s) - mitochondrion , diazoxide , reactive oxygen species , microbiology and biotechnology , excitotoxicity , adenosine triphosphate , chemistry , biophysics , biology , biochemistry , programmed cell death , apoptosis , endocrinology , insulin
Brain mitochondrial ATP‐sensitive K + channel (mitoK ATP ) opening by diazoxide protects against ischemic damage and excitotoxic cell death. Here we studied the redox properties of brain mitoK ATP . MitoK ATP activation during excitotoxicity in cultured cerebellar granule neurons prevented the accumulation of reactive oxygen species (ROS) and cell death. Furthermore, mitoK ATP activation in isolated brain mitochondria significantly prevented H 2 O 2 release by these organelles but did not change Ca 2+ accumulation capacity. Interestingly, the activity of mitoK ATP was highly dependent on redox state. The thiol reductant mercaptopropionylglycine prevented mitoK ATP activity, whereas exogenous ROS activated the channel. In addition, the use of mitochondrial substrates that led to higher levels of endogenous mitochondrial ROS release closely correlated with enhanced K + transport activity through mitoK ATP . Altogether, our results indicate that brain mitoK ATP is a redox‐sensitive channel that controls mitochondrial ROS release. © 2008 Wiley‐Liss, Inc.