Closed head injury increases extracellular levels of antioxidants in rat hippocampus in vivo: An adaptive mechanism?

Eitan Moor, Ron Kohen, Russel J. Reiter, Esther Shohami

Research output: Contribution to journalArticle

20 Scopus citations


Reactive oxygen species (ROS) are a major cause of secondary brain injury following head trauma. Low molecular weight antioxidants (LMWA) protect the tissue against oxidative damage caused by ROS. In the present study, we measured the extracellular levels of the LMWA ascorbic acid and uric acid in the rat brain before, during and after experimental closed head injury (CHI). A dialysis probe was inserted into the right ventral hippocampus through a chronically implanted guide. CHI was applied to the left hemisphere using a weight-drop device. CHI induced a rapid but transient increase in ascorbic acid levels. Uric acid levels increased to 250% of baseline shortly after CHI and remained elevated at 2 h after CHI. Previous results show that the overall reducing power of brain tissue decreases following CHI. Together with previous results, the current findings suggest that ascorbic acid and uric acid are mobilized from brain cells to the extracellular space.

Original languageEnglish (US)
Pages (from-to)169-172
Number of pages4
JournalNeuroscience Letters
Issue number3
StatePublished - Dec 28 2001



  • Antioxidants
  • Ascorbic acid
  • Closed head injury
  • Head trauma
  • Microdialysis
  • Oxidative stress
  • Uric acid

ASJC Scopus subject areas

  • Neuroscience(all)

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