Inhibiting Cytochrome C Oxidase Leads to Alleviated Ischemia Reperfusion Injury.
- Author:
Zhaoyun YANG
1
;
Zhongxin DUAN
;
Tian YU
;
Junmei XU
;
Lei LIU
Author Information
- Publication Type:Original Article
- Keywords: Ischemia-reperfusion injury; Cytochrome C oxidase; Mitochondria; Myocardial infarction
- MeSH: Animals; Cytochromes c*; Cytochromes*; Down-Regulation; Electron Transport Complex IV*; Infarction; Ischemia*; Mitochondria; Myocardial Infarction; Oxidative Stress; Potassium Cyanide; Rats; Reactive Oxygen Species; Reperfusion Injury*
- From:Korean Circulation Journal 2017;47(2):193-200
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND AND OBJECTIVES: The overall purpose of this study was to investigate the role of cytochrome C oxidase (CcO) in preventing ischemia reperfusion-induced cardiac injury through gaseous signaling molecule pathways. MATERIALS AND METHODS: We used CcO inhibitor, potassium cyanide (KCN) to mimic the pre-treatment of gaseous signaling molecules in a global ischemia/reperfusion (IR) injury model in rats. Intracellular reactive oxygen species (ROS) was determined by measuring mitochondrial H2O2 and mitochondrial complex activity. RESULTS: KCN pre-treatment led to decreased infarction area after IR injury and improved cardiac function. KCN pre-treated group challenged with IR injury was associated with reduced ROS production through inhibition of activity and not downregulation of CcO expression. In addition, KCN pre-treatment was associated with enhanced expression and activity of mitochondrial antioxidase, suggesting the role of CcO in regulating IR injury through oxidative stress. CONCLUSION: KCN pre-treatment reduced the severity of IR injury. The potential mechanism could be increased endogenous anti-oxidase activity and consequently, the enhanced clearance of ROS.
