Abstract
Nitrosative stress has been implicated in a large number of neurological disorders. The molecular mechanisms underlying the neuronal injury associated with this stimulus, however, are not clearly understood. Emerging evidence suggests that the liberation of intracellular zinc as well as over-activation of potassium channels may be two important components of nitrosative stress-induced neuronal death.
Copyright 2004 Springer-Verlag
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Apoptosis / drug effects
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Apoptosis / physiology*
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Humans
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Neurons / drug effects
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Neurons / metabolism*
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Neurons / pathology
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Oxidative Stress / physiology*
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Peroxynitrous Acid / adverse effects
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Peroxynitrous Acid / metabolism
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Potassium Channels, Voltage-Gated / drug effects
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Potassium Channels, Voltage-Gated / metabolism*
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Tyrosine / adverse effects
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Tyrosine / analogs & derivatives*
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Tyrosine / metabolism
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Zinc / metabolism*
Substances
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Potassium Channels, Voltage-Gated
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Peroxynitrous Acid
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3-nitrotyrosine
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Tyrosine
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Zinc