Background: Experimental data indicate that destructive oxidative events reach their peak within the first 24 h after trauma in head injury (HI) and that brain damage occurring due to this impact can be the cause of death or irreversible permanent disabilities in affected patients. Methods: Venous blood samples were obtained from 50 HI patients within 24 h of trauma onset and from 30 age- and sex-matched normal controls (NC). Patients were divided into three different neurological outcome groups: those who died within 10 days of trauma (D), and those with severe neurological deficits (SD) or mild/no neurological deficits (MD) at 90 days after trauma. Early oxidative changes in erythrocytes were assessed by estimating an indicator of lipid peroxidative damage - thiobarbituric acid-reactive substances (TBARS) - and antioxidants [reduced glutathione (GSH) levels and superoxide dismutase (SOD) activity]. Results: In the D group, erythrocyte TBARS levels were significantly higher compared to the NC, SD and MD groups (p<0.001); GSH levels were significantly lower compared to the NC (p<0.001) and MD (p<0.01) groups and SOD activity was significantly higher than in the NC (p<0.01) and MD (p<0.01) groups. In the SD group, TBARS levels were significantly higher than in the NC (p<0.001) and MD (p<0.05) groups; GSH levels were significantly lower than in the NC (p<0.001) and MD (p<0.01) groups and SOD activity was higher compared to the NC and MD (p<0.01) groups. In the MD group, TBARS levels were significantly higher and GSH levels significantly lower compared to the NC group (p<0.001). However, we did not observe any significant change in SOD activity compared to the NC group. Conclusions: These findings indicate that early oxidative changes may reflect the severity of neurological insult and provide an early indication of patient outcome in traumatic HI.
All Science Journal Classification (ASJC) codes
- Clinical Biochemistry
- Biochemistry, medical