Status of oxidant and antioxidants in term newborns with hypoxic ischemic encephalopathy: A case control design
Abstract
Hypoxic ischemic encephalopathy (HIE) is due to failure to initiate and sustain breathing immediately after delivery which may leads to increase mortality and morbidity in these neonates. This may cause severe and permanent neuropsychological sequelae, including mental retardation, visual motor or visual perceptive dysfunction, increased hyperactivity, cerebral palsy and epilepsy. The brain damage may occur due to release of free radicals in HIE. So this case control study was conducted on 50 neonates with HIE and 25 healthy neonates with the aim to compare the status of oxidants and antioxidants in these both groups. It was observed that Malonyldialdehyde (MDA) was found with significantly increased in study group than control group i.e. 12.26±4.1 nmol/ml in study and 2.10±0.10 nmol/ml in control group. Among antioxidants, Catalase (30.42± 7.7 v/s 14.59± 4.7) and SOD (2.59± 0.4 v/s 1.54± 0.3) were found significantly increased whereas Vit E (1.36± 0.3 v/s 2.73± 0.6) was found significantly decreased in neonates with HIE than controls.
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Introduction
Failure to initiate and sustain breathing immediately after delivery has been associated with hypoxic ischemic injury to the central nervous system (CNS) and the clinical manifestations of this injury have been termed as hypoxic ischemic encephalopathy (HIE). In India 9% of inborn babies has Apgar score of <7 at 1 minute and 1.5% of those suffer from Hypoxic ischemic encephalopathy (HIE).1
Perinatal hypoxic-ischemic encephalopathy (HIE) occurs in one to three per 1000 live full-term births. 2 Of affected newborns, 15%–20% die in the postnatal period and an additional 25% develop severe and permanent neuropsychological sequelae, including mental retardation, visual motor or visual perceptive dysfunction, increased hyperactivity, cerebral palsy, and epilepsy. 3
In HIE, free radicals are generated within mitochondria and also as by products in the synthesis of prostaglandins. These cause brain damage by attacking membranal fatty acids mainly polyunsaturated fatty acids (PUFA) and this is indicated by elevated levels of malonyldialdehyde (MDA). This process of damage to PUFA is knows as lipid peroxidation.4
Along with this, reduced antioxidative capacities of neonates may contribute to the pathogenesis of disorders in the perinatal period. Superoxide dismutase (SOD), Catalase and Vitamin E are three important antioxidants which help in protecting biological structures from free radical mediated injury.5
So this present study was conducted to elucidate the alterations in the expressions of superoxide dismutase(SOD), catalase, vitamin E and the levels of malonyldialdehyde as an index of lipid peroxidation (LPO) during HIE in comparison to control neonates.
Conclusion
This present study concludes that oxinants and antioxidants status was significantly altered in neonates with Hypoxic ischemic encephalopathy (HIE). Malonyldialdehyde (MDA) in study and control group was found significant increased in neonates with HIE than healthy neonates. Among antioxidants, Catalase and SOD were found significantly increased whereas Vit E was found significantly decreased in neonates with HIE than controls.