Brain damage after hypoxia-ischemia (HI) occurs in an age-dependent manner. Neuroprotective strategies assumed to be effective in the adult might have deleterious effects in the immature brain. In order to create effective therapies, the complex pathophysiology of HI in developing brain requires exploring new mechanisms. Critical determinants of neuronal survival after HI are the extent of vascular dysfunction, inflammation, and oxidative stress, followed later by tissue repair. The key enzyme of these processes in human body is arginase (ARG) that acts via bioavailability of nitric oxide, and synthesis of polyamines and proline. ARG is expressed throughout the brain in different cells, however, little is known about the effect of ARG in pathophysiological states of brain, especially hypoxia-ischemia. Here, we summarize the role of ARG during neurodevelopment, as well as in various brain pathologies.

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