Oxidative stress in brain according to traumatic brain injury intensity

J Surg Res. 2010 Dec;164(2):316-20. doi: 10.1016/j.jss.2009.04.031. Epub 2009 May 19.


Background: The mechanisms of brain damage and neuroplasticity following traumatic brain injury (TBI) are complex and not completely understood. Thus, we investigated markers of oxidative stress in the central nervous system after mild and severe TBI in rats.

Material and methods: Adult male wistar rats (five animals per group) submitted to mild (mTBI group) or severe TBI (sTBI Group) were sacrificed 30 min, 3, 6, or 12 h after the injury to quantify markers of oxidative damage in different brain regions. Levels of thiobarbituric acid reactive species and protein carbonyl in the cortex, hippocampus, striatum, and cerebellum of mTBI and sTBI groups were compared with the control group.

Results: After mTBI, levels of protein oxidation were increased in all analyzed structures in several different times after injury. The increase in TBARS levels was not so consistent in mTBI. In contrast, sTBI did not induce a sustainable increase in oxidative damage markers in all analyzed structures.

Conclusions: Oxidative damage seemed to be inversely proportional to severity of traumatic brain injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers
  • Brain Injuries / physiopathology*
  • Cerebral Cortex / physiopathology
  • Male
  • Oxidative Stress*
  • Protein Carbonylation
  • Rats
  • Rats, Wistar
  • Thiobarbituric Acid Reactive Substances / metabolism


  • Biomarkers
  • Thiobarbituric Acid Reactive Substances