Nitrosative stress and potassium channel-mediated neuronal apoptosis: is zinc the link?
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.
Pal
Sumon
S
Department of Neurobiology, University of Pittsburgh School of Medicine, E1456 BST, Pittsburgh, PA 15261, USA.
He
Kai
K
Aizenman
Elias
E
D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D009474:Neurons / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology*; D030421:Peroxynitrous Acid / Q000009:adverse effects / Q000378:metabolism; D024642:Potassium Channels, Voltage-Gated / Q000187:drug effects / Q000378:metabolism*; D014443:Tyrosine / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000378:metabolism; D015032:Zinc / Q000378:metabolism*
D024642:Potassium Channels, Voltage-Gated; D030421:Peroxynitrous Acid; C002744:3-nitrotyrosine; D014443:Tyrosine; D015032:Zinc