title: Evaluation of acetylcholinesterase and adenosine deaminase activities in brain and erythrocytes and proinflammatory cytokine levels in rats submitted to neonatal hypoxia-ischemia model.
abstract: Perinatal hypoxic-ischemic (HI) brain injury is a common problem with severe neurologic sequelae. The definitive brain injury is a consequence of pathophysiological mechanisms that begin at the moment of HI insult and may extend for days or weeks. In this context, the inflammatory response and the formation of reactive oxygen species seem to play a key role during evolution of brain damage after injury. Thus, the aim of this study was to describe the chronological sequence of acetylcholinesterase (AChE) activity and the lipid peroxidation changes in the cerebral cortex using the classic model of neonatal HI. Furthermore, the erythrocyte AChE and adenosine deaminase (ADA) activities as well as the serum levels of proinflammatory cytokines were assessed. We observed that neonatal HI caused an increase of lipid peroxidation immediately after HI insult, which remained for several days afterward. There was a time-related change in the AChE activity in the cerebral cortex and the same was observed in erythrocyte AChE and ADA activities. In addition, immediately after HI, ADA activity showed a strong positive correlation with all proinflammatory cytokines assessed. Together, these findings may help the understanding of some mechanism related to the pathophysiology of neonatal HI, therefore highlighting the putative therapeutic targets to minimize brain injury and enhance recovery.
authors.affiliation: Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Campus Universitário, Camobi, Santa Maria, RS, Brazil. victor.capi@yahoo.com.br
authors.forename: Victor Camera
authors.initials: VC
authors.lastname: Pimentel
authors.forename: Jéssica Lopes
authors.initials: JL
authors.lastname: Gomes
authors.forename: Daniela
authors.initials: D
authors.lastname: Zanini
authors.forename: Fátima Husein
authors.initials: FH
authors.lastname: Abdalla
authors.forename: Pauline
authors.initials: P
authors.lastname: da Costa
authors.forename: Jamile Fabbrin
authors.initials: JF
authors.lastname: Gonçalves
authors.forename: Marta Maria Medeiros Frescura
authors.initials: MM
authors.lastname: Duarte
authors.forename: Maria Beatriz
authors.initials: MB
authors.lastname: Moretto
authors.forename: Vera Maria
authors.initials: VM
authors.lastname: Morsch
authors.forename: Maria Rosa Chitolina
authors.initials: MR
authors.lastname: Schetinger
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism*; D000243:Adenosine Deaminase / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn; D002545:Brain Ischemia / Q000097:blood / Q000201:enzymology*; D015687:Cell Hypoxia; D002540:Cerebral Cortex / Q000098:blood supply / Q000201:enzymology*; D016207:Cytokines / Q000097:blood*; D004912:Erythrocytes / Q000201:enzymology*; D018836:Inflammation Mediators / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D051381:Rats; D017208:Rats, Wistar
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D000110:Acetylcholinesterase; D000243:Adenosine Deaminase