Redox properties of the adenoside triphosphate-sensitive K+ channel in brain mitochondria

✍ Scribed by Maynara Fornazari; Juliana G. de Paula; Roger F. Castilho; Alicia J. Kowaltowski

• Publisher: John Wiley and Sons
• Year: 2008
• Tongue: English
• Weight: 455 KB
• Volume: 86
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.21614

✦ Synopsis

Abstract

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.