Evaluation of mitochondrial respiratory chain in the brain of rats after pneumococcal meningitis.

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.