SOD2 Mediates Amifostine-Induced Protection against Glutamate in PC12 Cells

Figure 7

Hypothetical model of SOD2 mediates amifostine-induced neuroprotection against oxidative stress injury. Amifostine exposure increases mitochondrial SOD2 activity, which then consumes mitochondrial superoxide production induced by oxidative stress. Due to the depletion of mitochondrial superoxide production, intracellular ROS level is reduced, and GSH and CAT levels are restored, leading to an inhibition of oxidative stress injury and neuroprotection.