Introduction. The pathogenesis of perinatal hypoxic-ischemic brain damage is
highly complex. Objective. The aim of this study was to assess the role of
oxidative stress in hypoxic-ischemic brain injury and subsequent abnormal
neurological outcome in infants with perinatal hypoxic-ischemic
encephalopathy (HIE). We estimated perinatal oxidative brain damage measuring
activity of glutathione peroxidase (GPX) in cerebrospinal fluid (CSF) as an
indirect biomarker of free radical production during cerebral
hypoxia-ischemia in correlation with the level of intracellular enzyme neuron
specific enolase (NSE) in CSF as a biomarker of extend of brain injury.
Methods. Ninety neonates (>32 GA) with perinatal HIE were enrolled
prospectively. HIE was categorized into three stages according Sarnat and
Sarnat clinical scoring system and changes seen on amplitude integrated EEG.
CSF for GPX analysis and NSE analysis was taken in the first 72 hours of
life. Neurodevelopment outcome was assessed at 12 months of corrected
gestational age. Results. GPX activity in CSF was in good relation with
clinical stage of HIE (p<0.0001) and GA (p<0.0001) and significantly
corresponded with subsequent neurodevelopment outcome (p<0.001). GPX activity
in CSF showed a strong correlation with NSE levels in CSF (p<0.001) as the
biomarker of extent of brain injury. Conclusion. Our results suggest that
oxidative stress might be important contributing factor in perinatal
hypoxic-ischemic brain damage, particularly in preterm neonates.
Insights into the role of iron in immature rat model of hypoxic-ischemic brain injury