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

研究成果: Review article査読

493 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)1505-1517
ページ数13
ジャーナルAntioxidants and Redox Signaling
14
8
DOI
出版ステータスPublished - 2011 4 15

ASJC Scopus subject areas

  • 生化学
  • 生理学
  • 分子生物学
  • 臨床生化学
  • 細胞生物学

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