Abstract
K(+) channel openers can activate K channels and have been shown to protect cultured neurons against excitotoxicity. Our study showed that diazoxide, a K(+) channel opener, could counteract the effects of A beta(1-42) and protect cells from A beta(1-42)-induced the increasing of mitochondrial membrane potential and the associated increase in intracellular reactive oxygen species levels; an inducible nitric oxide synthase inhibitor, N omega-nitro-L-arginine could protect cells from A beta(1-42)-induced the increasing of both mitochondrial membrane potential and intracellular reactive oxygen species levels. A 24 h exposure to A beta(1-42) did not result in apoptosis, suggesting that the increase in both mitochondrial membrane potential and reactive oxygen species levels preceded cell apoptosis or death.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyloid beta-Peptides / antagonists & inhibitors*
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Amyloid beta-Peptides / toxicity*
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Cell Line, Tumor
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Cell Survival / drug effects
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Cell Survival / physiology
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Diazoxide / pharmacology*
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Dose-Response Relationship, Drug
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Humans
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Membrane Potentials / drug effects
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Membrane Potentials / physiology
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Mitochondria / drug effects
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Mitochondria / physiology
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Nitric Oxide Synthase / antagonists & inhibitors
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Nitric Oxide Synthase / metabolism
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Nitric Oxide Synthase Type II
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Nitroarginine / pharmacology*
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Peptide Fragments / antagonists & inhibitors*
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Peptide Fragments / toxicity*
Substances
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Amyloid beta-Peptides
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Peptide Fragments
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amyloid beta-protein (1-42)
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Nitroarginine
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NOS2 protein, human
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type II
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Diazoxide