Conformational change of mitochondrial complex I increases ROS sensitivity during ischemia.

ABSTRACT:

Aims

Myocardial ischemia/reperfusion (I/R) is associated with mitochondrial dysfunction and subsequent cardiomyocyte death. The generation of excessive quantities of reactive oxygen species (ROS) and resultant damage to mitochondrial enzymes is considered an important mechanism underlying reperfusion injury. Mitochondrial complex I can exist in two interconvertible states: active (A) and deactive or dormant (D). We have studied the active/deactive (A/D) equilibrium in several tissues under ischemic conditions in vivo and investigated the sensitivity of both forms of the heart enzyme to ROS.

Results

We found that in the heart, t½ of complex I deactivation during ischemia was 10 min, and that reperfusion resulted in the return of A/D equilibrium to its initial level. The rate

SUBMITTER: Gorenkova N 

PROVIDER: S-EPMC3797456 | biostudies-literature | 2013 Nov

REPOSITORIES: biostudies-literature