Hemispheric analysis of mitochondrial Complex I and II activity in the mouse model of ischemia-reperfusion-induced injury.

Brain ischemia/reperfusion injury results in a variable mixture of cellular damage, but little is known about possible patterns of mitochondrial dysfunction from the scope of hemispheric processes. The current study used high-resolution fluorespirometry to compare ipsi- and contralateral hemispheres' linked respiration and ROS emission after 60-minutes of filament induced middle cerebral artery occlusion (fMCAo) and 2, 24, 72, and 168 h after reperfusion in mice. Our findings highlight that experimental ischemic stroke resulted in higher mitochondrial respiration in the contralateral compared to the ipsilateral hemisphere and highest ROS emission in ipsilateral hemisphere. The largest difference between the ipsilateral and contralateral hemispheres was observed 2 h after reperfusion in Complex I and II ETS state. Oxygen flux returns to near baseline 72 h after reperfusion without any changes thereafter in Complex I and II respiration. Studying the effects of brain mitochondrial functionality after ischemic stroke in each cerebral hemisphere separately provides a better understanding about the molecular and compensatory processes of the contralateral hemisphere, a region of the brain often neglected in stroke research.