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Nitric oxide neurotoxicity

V L Dawson1, T M Dawson

  • 1Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA. valina_dawson@qmail.bs.jhu.edu

Journal of Chemical Neuroanatomy
|June 1, 1996
PubMed
Summary
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Glutamate excitotoxicity in neurodegenerative diseases involves nitric oxide (NO) overproduction, leading to cell damage. This excess NO, reacting with superoxide, forms peroxynitrite, a key mediator of neurotoxicity and oxidative stress in brain disorders.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Glutamate neurotransmission derangements are linked to neurodegenerative diseases like stroke, Alzheimer's, and ALS.
  • Activation of NMDA receptors leads to calcium influx, activating nNOS and producing nitric oxide (NO).

Purpose of the Study:

  • To elucidate the role of nitric oxide (NO) and peroxynitrite (ONOO-) in glutamate-induced neurotoxicity.
  • To highlight the susceptibility of the brain to oxidative stress in neurologic disorders.

Main Methods:

  • Review of scientific literature on glutamate excitotoxicity and oxidative stress.
  • Analysis of biochemical pathways involving NMDA receptors, NO, and peroxynitrite.

Main Results:

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  • Excess NO production contributes significantly to glutamate neurotoxicity.
  • Peroxynitrite, formed from NO and superoxide, is a major neurotoxic agent.
  • Brain's high lipid content and energy demands increase vulnerability to oxidative damage.

    • Conclusions:

    • Glutamate excitotoxicity involves NO and peroxynitrite, contributing to neuronal damage in neurodegenerative diseases.
    • Oxidative stress and free radical damage are significant components of many neurologic disorders.