Figure 2.

The interaction between zinc and ROS in ischemic stroke. In ischemic stroke, zinc is released from sources such as the synaptic vesicles of glutamatergic neurons. Acutely, zinc may elevate ROS through action on mitochondria. In the chronic phase, zinc accumulation can activate neuronal NADPH oxidases to generate additional oxidative species. The resultant ROS may produce neurotoxicity, further increasing zinc accumulation and ischemic brain injury. Note that while we show a central role for ROS, other mechanisms of zinc toxicity exist and are described in the text.