Kiris, TGörgülü, AÜnal, FTürkoglu, ÜÇobanoglu, SEkuklu, G2024-06-122024-06-1219990300-9130https://doi.org/10.1007/s004330050116https://hdl.handle.net/20.500.14551/19924Free radicals, lipid peroxidation and excitatory amino acids have been implicated in the secondary mechanisms of traumatic brain injury. We used the cold injury model in rats to assess the endogenous activity of the protective enzyme superoxide dismutase (SOD) and the lipid peroxidation level in the contused tissue at an early phase of injury. Furthermore, we treated the rats with two different N-methyl-D-aspartate receptor antagonists, namely MK-801 and CPP, and evaluated their effect on lipid peroxidation in the contused tissue. Rats were divided into four groups: sham, control, treatment 1 and treatment 2 groups (n = 16 for each group). Thirty and 60 min after craniectomy or injury, tissue samples were removed. SOD activity didn't change in this period. However, lipid peroxidation in terms of malondialdehyde (MDA) amount showed a significant increase at 60 min. Fifteen minutes after injury, MK-801 (1 mg/kg), CPP (10 mg/kg) or saline (1 ml) were applied intraperitoneally in treatment 1, treatment 2 and the control groups, Treatment with MK-801 attenuated MDA levels, whereas treatment with CPP did not. The protective effect of MK-801 achieved statistical significance. These results demonstrate that SOD activity does not change in the Parry period of cold injury. Moreover, these results show that lipid peroxidation increases after 60 min of cold injury, and treatment with MK-801 15 min after injury can prevent this elevation.en10.1007/s004330050116info:eu-repo/semantics/closedAccessCold InjuryLipid PeroxidationMK-801NMDA AntagonistSuperoxide DismutaseSpinal-Cord InjuryVasogenic Brain EdemaOxygen Free-RadicalsAmino-Acid ReleaseNeurological DisordersIschemiaExcitotoxicityInvolvementGlutamateReceptorsArticle1986341347Q3WOS:0000803255000052-s2.0-003293219910369089N/A