Hypoxic-Ischemic Injury in the Developing Brain: The Role of Reactive Oxygen Species Originating in Mitochondria

Figure 3

Proposed mechanisms of HI injury targeted by mitochondrial ROS and mechanisms of ROS generation in the MRC at the end of HI insult (a), at the initiation of a natural reperfusion (b), and the reperfusion therapeutically modified by an inhibition of the reperfusion-driven complex I recovery (c). Arrows indicate the leak of cytochrome c and apoptosis inducing factor (AIF), the loss of proton motive force and Ca⁺⁺ and ROS contribution to the mPTP opening. CsA is a cyclosporine A which partially inhibits mPTP.