Acute hypoxia-ischemia results in hydrogen peroxide accumulation in neonatal but not adult mouse brain.

The neonatal brain responds differently to hypoxic-ischemic injury and may be more vulnerable than the mature brain due to a greater susceptibility to oxidative stress. As a measure of oxidative stress, the immature brain should accumulate more hydrogen peroxide (H2O2) than the mature brain after a similar hypoxic-ischemic insult. To test this hypothesis, H2O2 accumulation was measured in postnatal day 7 (P7, neonatal) and P42 (adult) CD1 mouse brain regionally after inducing HI by carotid ligation followed by systemic hypoxia. H2O2 accumulation was quantified at 2, 12, 24, and 120 h after HI using the aminotriazole (AT)-mediated inhibition of catalase spectrophotometric method. Histologic injury was determined by an established scoring system, and infarction volume was determined. P7 and P42 animals were subjected to different durations of hypoxia to create a similar degree of brain injury. Despite similar injury, significantly less H2O2 accumulated in P42 mouse cortex compared with P7 at 2, 12, and 24 h after HI. In addition, less H2O2 accumulated in P42 mouse hippocampus compared with P7 hippocampus at 2 h. Since immature neurons are more vulnerable to the toxic effects of H2O2 than mature neurons, this increased accumulation in the immature brain may explain why the neonatal brain may be more devastated, even after a milder degree of acute hypoxic-ischemic injury.