Mitochondrial respiratory chain and creatine kinase activities following trauma brain injury in brain of mice preconditioned with N-methyl-d-aspartate

• Published in: Molecular and cellular biochemistry 2013-12, Vol.384 (1-2), p.129-137
• Main Authors: Boeck, Carina R., Carbonera, Leatrice S., Milioli, Mônia E., Constantino, Leandra C., Garcez, Michelle L., Rezin, Gislaine T., Scaini, Giselli, Streck, Emilio L.
• Format: Article
• Language: English
• Subjects: Animals; Aspartate; Biochemistry; Biomedical and Life Sciences; Brain; Brain damage; Brain Injuries - drug therapy; Brain Injuries - metabolism; Brain injury; Cardiology; Cerebellum - enzymology; Cerebellum - metabolism; Cerebral Cortex - enzymology; Cerebral Cortex - metabolism; Creatine kinase; Creatine Kinase - metabolism; Enzymatic activity; Enzymes; Excitatory Amino Acid Agonists - therapeutic use; Injuries; Kinases; Life Sciences; Male; Medical Biochemistry; Methyl aspartate; Mice; Mitochondria; Mitochondria - metabolism; Mitochondrial DNA; Mitochondrial Membranes - metabolism; N-Methylaspartate - therapeutic use; Neurochemistry; Oncology; Oxidative Stress - drug effects; Physiological aspects; Receptors, N-Methyl-D-Aspartate - metabolism; Rodents
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-013-1790-8

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.