RESUMO
The brain is highly dependent on ATP and most cell energy is obtained through oxidative phosphorylation, a process requiring the action of various respiratory enzyme complexes located in a special structure of the inner mitochondrial membrane. Bacterial meningitis due to Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae including sensory-motor deficits, seizures, and impairments of learning and memory. In this context, we evaluated the activities of mitochondrial respiratory chain complexes in the brain of rats submitted to meningitis by S. pneumoniae inoculation into the cisterna magna. Our results demonstrated that complex I activity was not altered in cerebral cortex after meningitis; complexes II, III and IV were increased 24 and 48h after meningitis. We have also verified that complex I was inhibited in prefrontal cortex 48h after meningitis; complexes II, III and IV were not altered. Our results also demonstrated that complex I activity was inhibited in striatum, hippocampus and cerebellum 24h after meningitis. Moreover, complex II activity was increased in hippocampus and striatum 24 and 48h after meningitis; complexes III and IV activity were increased in striatum, hippocampus and cerebellum 48h after meningitis. Taking together previous reports and our present findings, we speculate that oxidative stress and metabolism impairment might contribute, at least in part, for the pathogenesis of pneumococcal meningitis.
Assuntos
Encéfalo/enzimologia , Encéfalo/patologia , Complexo de Proteínas da Cadeia de Transporte de Elétrons/metabolismo , Meningite Pneumocócica/patologia , Mitocôndrias/enzimologia , Animais , Encéfalo/microbiologia , Modelos Animais de Doenças , Transporte de Elétrons/fisiologia , Masculino , Meningite Pneumocócica/fisiopatologia , Ratos , Ratos WistarRESUMO
Bacterial meningitis is associated with intense inflammation and also linked to the production of reactive oxygen species. To this aim, animals underwent a magna cistern tap and received either sterile saline as a placebo or an equivalent volume of a Streptococcus pneumoniae suspension. The animals began antibiotic therapy 16h after induction. The animals were sacrificed at 24 or 48h post-infection and the hippocampus and cortex were harvested. The activity of the enzymes superoxide dismutase, catalase, and thiobarbituric acid reactive species, protein carbonyls, and free sulphydryl groups were altered, but reversed, in part, by the antibiotic treatment. Our results support the hypothesis that antibiotic treatment prevents, in part, the oxidative stress in the bacterial meningitis induced by Streptococcus pneumoniae.