Oxidants and the central nervous system: some fundamental questions. Is oxidant damage relevant to Parkinson's disease, Alzheimer's disease, traumatic injury or stroke?

Oxidants and the central nervous system: some fundamental questions. Is oxidant damage relevant... Abstract– Radicals are species containing one or more unpaired electrons. The oxygen radical superoxide (O2‐) and the non‐radical oxidant hydrogen peroxide (H2O2) are produced during normal metabolism and perform several useful functions. Excessive production of O2‐ and H2O2 can result in tissue damage, which often involves generation of highly‐reactive hydroxyl radical (·OH) and other oxidants in the presence of “catalytic'’iron ions. A major form of antioxidant defence is the storage and transport of iron ions in forms that will not catalyze formation of reactive radicals. Tissue injury, eg. by ischaemia or trauma, can cause increased iron availability and accelerate free radical reactions. This may be especially important in the brain, since areas of this organ are rich in iron and cerebrospinal fluid cannot bind released iron ions. Oxidant stress upon nervous tissue can produce damage by several interacting mechanisms, including rises in intracellular free Ca2‐ and, possibly, release of excitatory amino acids. Recent suggestions that iron‐dependent free radical reactions are involved in the neurotoxicity of aluminium and in damage to the substantia nigra in Parkinson's disease are reviewed. Finally, the nature of antioxidants is discussed, it being suggested that antioxidant enzymes and chelators of iron ions may be more generally‐useful protective agents than chain‐breaking antioxidants. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Acta Neurologica Scandinavica Wiley

Oxidants and the central nervous system: some fundamental questions. Is oxidant damage relevant to Parkinson's disease, Alzheimer's disease, traumatic injury or stroke?

Acta Neurologica Scandinavica, Volume 80 – Nov 1, 1989

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Publisher
Wiley
Copyright
Copyright © 1989 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0001-6314
eISSN
1600-0404
D.O.I.
10.1111/j.1600-0404.1989.tb01779.x
Publisher site
See Article on Publisher Site

Abstract

Abstract– Radicals are species containing one or more unpaired electrons. The oxygen radical superoxide (O2‐) and the non‐radical oxidant hydrogen peroxide (H2O2) are produced during normal metabolism and perform several useful functions. Excessive production of O2‐ and H2O2 can result in tissue damage, which often involves generation of highly‐reactive hydroxyl radical (·OH) and other oxidants in the presence of “catalytic'’iron ions. A major form of antioxidant defence is the storage and transport of iron ions in forms that will not catalyze formation of reactive radicals. Tissue injury, eg. by ischaemia or trauma, can cause increased iron availability and accelerate free radical reactions. This may be especially important in the brain, since areas of this organ are rich in iron and cerebrospinal fluid cannot bind released iron ions. Oxidant stress upon nervous tissue can produce damage by several interacting mechanisms, including rises in intracellular free Ca2‐ and, possibly, release of excitatory amino acids. Recent suggestions that iron‐dependent free radical reactions are involved in the neurotoxicity of aluminium and in damage to the substantia nigra in Parkinson's disease are reviewed. Finally, the nature of antioxidants is discussed, it being suggested that antioxidant enzymes and chelators of iron ions may be more generally‐useful protective agents than chain‐breaking antioxidants.

Journal

Acta Neurologica ScandinavicaWiley

Published: Nov 1, 1989

References

  • Excitatory amino acid release from rat hippocampal slices as a consequence of free‐radical formation
    Pellegrini‐Giampietro, Pellegrini‐Giampietro; Cherichi, Cherichi; Alesiani, Alesiani; Carla, Carla; Moroni, Moroni
  • Mechanism of kainate toxicity to cerebellar neurons in vitro is analogous to reperfusion tissue injury
    Dykens, Dykens; Stern, Stern; Trenkner, Trenkner
  • Identification of hypoxanthine transport and xanthine oxidase activity in brain capillaries
    Betz, Betz
  • Transition metals, ferritin, glutathione and ascorbic acid in Parkinsonian brains
    Riederer, Riederer; Sofic, Sofic; Rausche, Rausche; Schmidt, Schmidt; Reynolds, Reynolds; Jallinger, Jallinger; Youdim, Youdim
  • Protective effects of liposome‐entrapped superoxide dismutase on posttraumatic brain edema
    Chan, Chan; Longar, Longar; Fishman, Fishman

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