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Updated: May 23, 2026

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
Published on: November 19, 2008
The role of oxidative stress in perinatal hypoxic-ischemic brain injury
Brankica Vasiljević1, Svjetlana Maglajlić-Djukić, Miroslava Gojnić
1Clinic of Gynecology and Obstetrics, Clinical Centre of Serbia Visgradska 26, 11000 Belgrade, Serbia. bdvasilj@eunet.rs
Insights
Oxidative stress, measured by glutathione peroxidase (GPX) in cerebrospinal fluid (CSF), is linked to brain injury severity and neurodevelopmental outcomes in infants with hypoxic-ischemic encephalopathy (HIE). This suggests a key role for oxidative stress in HIE pathogenesis.
Area of Science:
- Neonatal Neurology
- Biochemistry
- Neuroscience
Background:
- Perinatal hypoxic-ischemic encephalopathy (HIE) is a complex condition.
- Understanding its pathogenesis is crucial for improving infant outcomes.
Purpose of the Study:
- To investigate the role of oxidative stress in HIE.
- To correlate oxidative stress markers with brain injury extent and neurological outcomes.
- To assess glutathione peroxidase (GPX) and neuron-specific enolase (NSE) in CSF as biomarkers.
Main Methods:
- Prospective study of 90 neonates with HIE (gestational age >32 weeks).
- Categorization of HIE severity using Sarnat and Sarnat criteria and amplitude-integrated EEG.
- Measurement of CSF GPX activity and NSE levels within 72 hours of birth.
- Neurodevelopmental assessment at 12 months corrected gestational age.
Main Results:
- CSF GPX activity correlated significantly with HIE clinical stage and gestational age.
- GPX activity strongly correlated with NSE levels, indicating extent of brain injury.
- GPX activity in CSF predicted subsequent neurodevelopmental outcomes.
Conclusions:
- Oxidative stress appears to be a significant factor in perinatal hypoxic-ischemic brain damage.
- This is particularly relevant in preterm neonates.
- GPX activity serves as a valuable biomarker for assessing HIE severity and prognosis.
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.
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