3,4Uludag University School of Medicine, Department of Biochemistry, Bursa, Turkey AIM: HI (hypoxic–ischemic) brain injury is a major cause of neonatal mortality and longterm neurological morbidity. The aim of the present study was to investigate the effects of HPC (hypoxic preconditioning) on the oxidative-antioxidative status in the neonatal HI brain model.
MATERIAL and METHODS: Fifty five 7-day-old rats were placed into; Control, HPC, HPC+HI insult, and HI insult groups. HPC, The HPC+HI insult groups were subjected to hypoxia (37°C, 8%O2) and the control group to normoxia for 2.5 hrs. Twenty-four hours later, the rats in the HPC+HI insult and HI insult groups were exposed to cerebral HI produced by unilateral right common carotid artery (CCA) occlusion combined with 90 min hypoxia. Four hours after recovery, the malondialdehyde (MDA) level and the activities of superoxide dismutase (SOD), and glutathione peroxidase (GPx) were determined in the brain tissues of the rats.
RESULTS: The findings of the present study suggest increased lipid peroxidation and/or decreased antioxidant activity in the brain of the HI rats.
CONCLUSION: The beneficial effects of HPC might not be related to the alterations in the antioxidative activity.
Keywords : Antioxidant enzymes, Hypoxic ischemic brain damage, Lipid peroxidation, Neuroprotection, Preconditioning