Oxidative stress in ischemic brain damage: Mechanisms of cell death and potential molecular targets for neuroprotection

Hai Chen, Hideyuki Yoshioka, Gab Seok Kim, Joo Eun Jung, Nobuya Okami, Hiroyuki Sakata, Carolina M. Maier, Purnima Narasimhan, Christina E. Goeders, Pak H. Chan

Research output: Contribution to journalReview article

442 Citations (Scopus)

Abstract

Significant amounts of oxygen free radicals (oxidants) are generated during cerebral ischemia/reperfusion, and oxidative stress plays an important role in brain damage after stroke. In addition to oxidizing macromolecules, leading to cell injury, oxidants are also involved in cell death/survival signal pathways and cause mitochondrial dysfunction. Experimental data from laboratory animals that either overexpress (transgenic) or are deficient in (knock-out) antioxidant proteins, mainly superoxide dismutase, have provided strong evidence of the role of oxidative stress in ischemic brain damage. In addition to mitochondria, recent reports demonstrate that NADPH oxidase (NOX), an important pro-oxidant enzyme, is also involved in the generation of oxidants in the brain after stroke. Inhibition of NOX is neuroprotective against cerebral ischemia. We propose that superoxide dismutase and NOX activity in the brain is a major determinant for ischemic damage/repair and that these major anti- and pro-oxidant enzymes are potential endogenous molecular targets for stroke therapy.

Original languageEnglish
Pages (from-to)1505-1517
Number of pages13
JournalAntioxidants and Redox Signaling
Volume14
Issue number8
DOIs
Publication statusPublished - 2011 Apr 15

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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    Chen, H., Yoshioka, H., Kim, G. S., Jung, J. E., Okami, N., Sakata, H., Maier, C. M., Narasimhan, P., Goeders, C. E., & Chan, P. H. (2011). Oxidative stress in ischemic brain damage: Mechanisms of cell death and potential molecular targets for neuroprotection. Antioxidants and Redox Signaling, 14(8), 1505-1517. https://doi.org/10.1089/ars.2010.3576