title: Oxidative variables in the rat brain after sepsis induced by cecal ligation and perforation.
abstract: OBJECTIVE
  The underlying mechanisms of the changes in mental status, septic encephalopathy, and long-term cognitive symptoms in sepsis survivors have only been defined in part. The present study was undertaken to assess different variables of oxidative stress in several brain structures after cecal ligation and perforation in the rat.
  
  
  METHODS
  Prospective animal study.
  
  
  METHODS
  Animal basic science laboratory.
  
  
  METHODS
  Male Wistar rats, weighing 250-350 g.
  
  
  METHODS
  Rats were subjected to cecal ligation and perforation (sepsis group) with saline resuscitation (at 50 mL/kg immediately and 12 hrs after cecal ligation and perforation) or sham operation (control group).
  
  
  RESULTS
  Oxidative damage, assessed by the thiobarbituric acid reactive species and the protein carbonyl assays, occurred early (after 6 hrs) in the course of sepsis development in the hippocampus, cerebellum, and cortex. At longer times after sepsis induction (12-96 hrs), there was no evidence of oxidative damage in all analyzed structures. Except for the striatum, earlier in sepsis development (6 hrs) we demonstrated an increase in superoxide dismutase activity without a proportional increase in catalase activity with a consequent increase in the relation of superoxide dismutase/catalase. The balance between these enzymes was restored in the studied structures 12-96 hrs after sepsis induction.
  
  
  CONCLUSIONS
  The short-term oxidative damage demonstrated here could participate in the development of central nervous system symptoms during sepsis development, or even septic encephalopathy. The alterations in the superoxide dismutase/catalase relation were temporally related to the occurrence or not of oxidative damage in the central nervous system.
authors.affiliation: Laboratório de Neurociências, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
authors.forename: Tatiana
authors.initials: T
authors.lastname: Barichello
authors.forename: Jucélia J
authors.initials: JJ
authors.lastname: Fortunato
authors.forename: Angeles M
authors.initials: AM
authors.lastname: Vitali
authors.forename: Gustavo
authors.initials: G
authors.lastname: Feier
authors.forename: Adalisa
authors.initials: A
authors.lastname: Reinke
authors.forename: José Cláudio F
authors.initials: JC
authors.lastname: Moreira
authors.forename: João
authors.initials: J
authors.lastname: Quevedo
authors.forename: Felipe
authors.initials: F
authors.lastname: Dal-Pizzol
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism; D001927:Brain Diseases / Q000209:etiology* / Q000503:physiopathology*; D002374:Catalase / Q000378:metabolism; D005609:Free Radicals / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress; D011446:Prospective Studies; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000150:complications*; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors
chemical_list: D005609:Free Radicals; D002374:Catalase; D013482:Superoxide Dismutase