title: Mitochondrial respiratory chain and creatine kinase activities following trauma brain injury in brain of mice preconditioned with N-methyl-D-aspartate.
abstract: Traumatic brain injury (TBI) induces glutamatergic excitotoxicity through N-methyl-D-aspartate (NMDA) receptors, affecting the integrity of the mitochondrial membrane. Studies have pointed to mitochondria as the master organelle in the preconditioning-triggered endogenous neuroprotective response. The present study is aimed at understanding energy metabolism in the brains of mice after preconditioning with NMDA and TBI. For this purpose, male albino CF-1 mice were pre-treated with NMDA (75 mg/kg) and subjected to brain trauma. Mitochondrial respiratory chain and creatine kinase activities were assessed at 6 or 24 h after trauma. The mice preconditioned and subjected to TBI exhibited augmented activities of complexes II and IV in the cerebral cortex and/or cerebellum. Creatine kinase activity was also augmented in the cerebral cortex after 24 h. We suggest that even though NMDA preconditioning and TBI have similar effects on enzyme activities, each manage their response via opposite mechanisms because the protective effects of preconditioning are unambiguous. In conclusion, NMDA preconditioning induces protection via an increase of enzymes in the mitochondria.
authors.affiliation: Laboratório de Biologia Celular e Molecular, Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), Programa de Pós-Graduação em Ciências da Saúde (PPGCS), Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense (UNESC), Criciúma, SC, 88806-000, Brazil, cariboeck@hotmail.com.
authors.forename: Carina R
authors.initials: CR
authors.lastname: Boeck
authors.forename: Leatrice S
authors.initials: LS
authors.lastname: Carbonera
authors.forename: Mônia E
authors.initials: ME
authors.lastname: Milioli
authors.forename: Leandra C
authors.initials: LC
authors.lastname: Constantino
authors.forename: Michelle L
authors.initials: ML
authors.lastname: Garcez
authors.forename: Gislaine T
authors.initials: GT
authors.lastname: Rezin
authors.forename: Giselli
authors.initials: G
authors.lastname: Scaini
authors.forename: Emilio L
authors.initials: EL
authors.lastname: Streck
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000188:drug therapy* / Q000378:metabolism*; D002531:Cerebellum / Q000201:enzymology / Q000378:metabolism; D002540:Cerebral Cortex / Q000201:enzymology / Q000378:metabolism; D003402:Creatine Kinase / Q000378:metabolism*; D018690:Excitatory Amino Acid Agonists / Q000627:therapeutic use; D008297:Male; D051379:Mice; D008928:Mitochondria / Q000378:metabolism*; D051336:Mitochondrial Membranes / Q000378:metabolism*; D016202:N-Methylaspartate / Q000627:therapeutic use*; D018384:Oxidative Stress / Q000187:drug effects; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism
chemical_list: D018690:Excitatory Amino Acid Agonists; D016194:Receptors, N-Methyl-D-Aspartate; D016202:N-Methylaspartate; D003402:Creatine Kinase