Role of arginase in hypoxic–ischemic brain injury in infants: An update

Hypoxic–ischemic (HI) brain injury is a major cause of neurological impairment in newborns worldwide and can lead to severe short- and long-term neurodevelopmental dysfunction. Adult neuroprotective interventions, on the other hand, may have a major influence on children’s developing nervous systems. The detailed aetiology of HI in the developing brain needs to be discovered to establish new pathways for successful therapies. The exact mechanism of newborn HI brain damage is still not completely known. However, mitochondria play a huge part not only because of their central position in metabolism, but also because certain enzymes are involved in the mitochondrial urea cycle. Arginase is responsible for two key physiological functions: the production of proline and polyamines, and the detoxification of ammonium ions. The arginase enzyme catalyses the final phase of the urea cycle by removing extra nitrogen from the amino acid. The release of nitrogen is a key feature of both neuronal and vascular cell signalling and is crucial for ensuring adequate blood supply to the central nervous system. In this mini-review, arginine and ornithine were used to evaluate their roles in regulating arginase activity under HI conditions.