Neuroprotective effect of an antioxidant in ischemic brain injury: Involvement of neuronal apoptosis

Miki Fujimura, Teiji Tominaga, Pak H. Chan

Research output: Contribution to journalArticlepeer-review

73 Citations (Scopus)

Abstract

The production of reactive oxygen species (ROS) has been implicated in reperfusion injury after cerebral ischemia, and antioxidant enzymes are believed to be among the major mechanisms by which the cells counteract the deleterious effect of ROS after cerebral ischemia. ROS also mediate the mitochondrial signaling pathway that may lead to apoptosis following cerebral ischemia. The recent development and availability of transgenic and knockout mutant rodents that either overexpress or are deficient in antioxidant genes have provided powerful tools for dissecting the molecular and cellular mechanisms of signaling pathways, direct oxidative damage, or both that are involved in ischemic brain injury. This article focuses on the contribution of ROS or an antioxidant system to the molecular pathway of postischemic apoptosis following transient focal cerebral ischemia by using transgenic mice that overexpress the cytosolic antioxidant copper/zinc superoxide dismutase.

Original languageEnglish
Pages (from-to)59-66
Number of pages8
JournalNeurocritical Care
Volume2
Issue number1
DOIs
Publication statusPublished - 2005

Keywords

  • Apoptosis
  • DNA damage
  • Focal cerebral ischemia
  • Reperfusion injury
  • Superoxide dismutase

ASJC Scopus subject areas

  • Clinical Neurology
  • Critical Care and Intensive Care Medicine

Fingerprint Dive into the research topics of 'Neuroprotective effect of an antioxidant in ischemic brain injury: Involvement of neuronal apoptosis'. Together they form a unique fingerprint.

Cite this