Media type: E-Article Title: Redox properties of the adenoside triphosphate‐sensitive K+ channel in brain mitochondria Contributor: Fornazari, Maynara; de Paula, Juliana G.; Castilho, Roger F.; Kowaltowski, Alicia J. imprint: Wiley, 2008 Published in: Journal of Neuroscience Research Language: English DOI: 10.1002/jnr.21614 ISSN: 0360-4012; 1097-4547 Keywords: Cellular and Molecular Neuroscience Origination: Footnote: Description: <jats:title>Abstract</jats:title><jats:p>Brain mitochondrial ATP‐sensitive K<jats:sup>+</jats:sup> channel (mitoK<jats:sub>ATP</jats:sub>) opening by diazoxide protects against ischemic damage and excitotoxic cell death. Here we studied the redox properties of brain mitoK<jats:sub>ATP</jats:sub> . MitoK<jats:sub>ATP</jats:sub> activation during excitotoxicity in cultured cerebellar granule neurons prevented the accumulation of reactive oxygen species (ROS) and cell death. Furthermore, mitoK<jats:sub>ATP</jats:sub> activation in isolated brain mitochondria significantly prevented H<jats:sub>2</jats:sub>O<jats:sub>2</jats:sub> release by these organelles but did not change Ca<jats:sup>2+</jats:sup> accumulation capacity. Interestingly, the activity of mitoK<jats:sub>ATP</jats:sub> was highly dependent on redox state. The thiol reductant mercaptopropionylglycine prevented mitoK<jats:sub>ATP</jats:sub> 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<jats:sup>+</jats:sup> transport activity through mitoK<jats:sub>ATP</jats:sub> . Altogether, our results indicate that brain mitoK<jats:sub>ATP</jats:sub> is a redox‐sensitive channel that controls mitochondrial ROS release. © 2008 Wiley‐Liss, Inc.</jats:p>