Preconditioning with prolonged normobaric hyperoxia induces ischemic tolerance partly by upregulation of antioxidant enzymes in rat brain tissue.

Recent studies suggest that normobaric hyperoxia (HO) results in brain ischemic tolerance (BIT), reducing ischemic brain injury. We have attempted to determine the time course of HO-induced upregulation of antioxidant enzymes. Rodents comprised five groups, breathing room air (RA; O(2)=21%), or 95% oxygen (hyperoxia, HO) for 4, 8, 16, and 24 h (RA, 4HO, 8HO, 16HO, 24HO respectively) in the same chamber. Each main group was subdivided to MCAO-operated (middle cerebral artery occlusion), and intact (without any surgery) subgroups. After 24 h, MCAO-operated subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit score (NDS), mortality rate, and infarct volume were measured in MCAO-operated subgroups. 48 h after pretreatment, antioxidant enzymes activities were assessed in MCAO-operated, sham-operated, and intact subgroups. Preconditioning with 16HO and 24HO decreased NDS, mortality rate, infarct volume, and increased antioxidant enzymes activities (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) significantly. Although further studies are needed to clarify the mechanisms of ischemic tolerance, the prolonged HO seems to partly exert their effects via increase in antioxidant enzymes activities.