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.