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

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

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 languageAmerican English
Pages (from-to)169-172
Number of pages4
JournalNeuroscience Letters
Volume316
Issue number3
DOIs
StatePublished - 28 Dec 2001

Bibliographical note

Funding Information:
The present work was supported by the Israeli Science Foundation (117/00) and the US–Israel Binational Science Foundation (#97-00259-2). E.M. is supported by a grant from the Golda Meir Fellowship Fund. R.K. and E.S. are affiliated with the David R. Bloom Center of Pharmacy.

Keywords

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

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