Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia.

Abstract

Reactive oxygen species have been implicated in brain injury after cerebral ischemia. These oxidants can damage proteins, lipids, and DNA, and lead to cell injury and necrosis. Oxidants are also initiators in intracellular cell death signaling pathways that may lead to apoptosis. The possible targets of this redox signaling include mitochondria, death membrane receptors, and DNA repair enzymes. Genetic manipulation of intrinsic antioxidants and the factors in the signaling pathways has provided substantial progress in understanding the mechanisms in cell death signaling pathways and involvement of oxygen radicals in ischemic brain injury. Future studies of these pathways may provide novel therapeutic strategies in clinical stroke.

• Authors: Taku Sugawara, Pak H Chan
• Journal: Antioxidants & redox signaling (Antioxid Redox Signal) Vol. 5 Issue 5 Pg. 597-607 (Oct 2003) ISSN: 1523-0864 [Print] United States
• PMID: 14580316 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., Review)

Chemical References

• Reactive Oxygen Species
• Glutathione Peroxidase
• Nitric Oxide Synthase
• Superoxide Dismutase
• APEX1 protein, human
• Apex1 protein, mouse
• DNA-(Apurinic or Apyrimidinic Site) Lyase

Topics

• Animals
• Apoptosis (physiology)
• Brain Ischemia (metabolism, physiopathology)
• Cell Death
• DNA-(Apurinic or Apyrimidinic Site) Lyase (physiology)
• Glutathione Peroxidase (metabolism)
• Humans
• Mice
• Mice, Knockout
• Mice, Transgenic
• Mitochondria (physiology)
• Models, Biological
• Neurons (metabolism)
• Nitric Oxide Synthase (metabolism)
• Reactive Oxygen Species (metabolism)
• Signal Transduction (physiology)
• Superoxide Dismutase (metabolism)