Impaired cortical energy metabolism but not major antioxidant defenses in experimental bacterial meningitis.

摘要: The loss of soluble brain antioxidants and protective effects radical scavengers implicate reactive oxygen species in cortical neuronal injury caused by bacterial meningitis. However, the lack significant oxidative damage cortex [J. Neuropathol. Exp. Neurol. 61 (2002) 605-613] suggests that may not be due to excessive parenchymal oxidant production. To see whether this tissue region exhibits a prooxidant state meningitis, we examined major antioxidant defenses infant rats infected with Streptococcus pneumoniae. Adenine nucleotides were co-determined assess possible changes energy metabolism. Arguing against heightened production, high NADPH/NADP(+) ratio ( approximately 3:1) activities defense pentose phosphate pathway enzymes remained unchanged at time fulminant In contrast, ATP, ADP total adenine on average decreased 25%. depletion did lead decrease adenylate charge (AEC). ATP was likely consequence metabolic degradation, since it correlated both accumulation purine degradation products. Furthermore, AEC significantly extent injury. These results strongly suggest rather than is involved observed