Ischemic preconditioning increases antioxidants in the brain and peripheral organs after cerebral ischemia

Lucio Glantz, Aharon Avramovich, Victoria Trembovler, Vladimir Gurvitz, Ron Kohen, Leonid A. Eidelman, Esther Shohami*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

59 Scopus citations


Background and purpose. Low molecular weight antioxidants (LMWA), which reflect tissue reducing power, are among the endogenous mechanisms for neutralizing reactive oxygen species (ROS). Ischemic preconditioning (IPC) was associated with decreased oxidative stress. We examined the effect of focal ischemia on LMWA and on prostaglandin E2 (PGE2, a product of arachidonic acid oxidation) in the brain, heart, liver, and lungs of rats subjected to 90 min of ischemia and in IPC rats subjected to similar insult. Methods. Transient right middle cerebral artery occlusion (MCAO) was performed for 90 min and at 0, 5, 30, 60, or 240 min of reperfusion, LMWA and PGE 2 were evaluated by cyclic voltametry (CV) and radioimmunoassay, respectively. IPC was induced by 2 min of MCAO, 24 h prior to the major ischemic episode. Results. LMWA decreased at 5 min of reperfusion in the brain, heart, liver, and lung and rose 4 h later only in the brain. PGE2 levels increased three to fivefold in all tissues examined. Surprisingly, in IPC rats a dramatic increase of LMWA occurred at 5 min of reperfusion in the brain and in the peripheral organs. Uric acid, but not ascorbic, is the major LMWA increased. Conclusions. We propose that after ischemia, ROS rapidly consume the antioxidants reserves in the brain and also in peripheral organs, suggesting that the whole body is under oxidative stress. Moreover, part of the neuroprotection afforded by IPC is mediated by the brain's ability to mobilize antioxidants, especially uric acid, that attenuate the massive ROS-mediated oxidative stress.

Original languageAmerican English
Pages (from-to)117-124
Number of pages8
JournalExperimental Neurology
Issue number1
StatePublished - Mar 2005

Bibliographical note

Funding Information:
The authors gratefully acknowledge the editorial assistance of Ms Gloria Ginzach. VT is supported by the Israel Ministry of absorption. ES and RK are affiliated with the David R. Bloom Center for Pharmaceutics, the HU school of Pharmacy, Jerusalem.


  • Ascorbic acid
  • Biological oxidation potential
  • Brain ischemia
  • Reactive oxygen species
  • Uric acid


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