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Adenosine deaminase activity,lipid peroxidation and astrocyte responses in the cerebral cortex of rats after neonatal hypoxia ischemia
Authors:VC Pimentel  LP Bellé  FV Pinheiro  KS De Bona  SCA Da Luz  MB Moretto
Institution:1. Postgraduate Program in Pharmaceutical Sciences, Health Science Centre, Santa Maria, RS, Brazil;2. Departamento de Análises Clínicas e Toxicológicas, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil;3. Department of Pathology, Federal University of Santa Maria, Santa Maria, RS, Brazil
Abstract:Hypoxia ischemia (HI) is a common cause of damage in the fetal and neonatal brain. Lifelong disabilities such as cerebral palsy, epilepsy, behavioral and learning disorders are some of the consequences of brain injury acquired in the perinatal periods. Inflammation and formation of free radicals appear to play key roles in neonatal HI. The aim of this study was to describe the chronological sequence of adenosine deaminase (ADA) activity, the oxidative damage changes and astrocyte response using the classic model of neonatal HI. We observed an increase in the activity of ADA and lipid peroxidation in the cerebral cortex 8 days after neonatal HI. This was accompanied by a GFAP-positive, and the degree of brain damage was determined histochemically by hematoxylin–eosin (HE). Taking into account the important anti-inflammatory role of adenosine, ADA may provide an efficient means for scavenging cell-surrounding adenosine and play an important part in subsequent events of neonatal HI in association with GFAP reactive gliosis. The present investigation showed that neonatal HI causes the increase of free radicals and significant damage in the cerebral cortex. The increase in ADA activity may reflect the activation of the immune system caused by HI because the morphological analysis exhibited a lymphocytic infiltration.
Keywords:Hypoxia ischemia  Adenosine deaminase  Cortex  Lipid peroxidation  GFAP
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