Abstract
Hydrogen sulfide (H2S) can enzymatically be produced from cysteine in the brain. H2S functions as a synaptic modulator as well as a neuroprotectant from oxidative stress in the brain. Here we show that H2S specifically enhances the reducing activity in neurons and mouse neuroblastoma Neuro2a cells. An inhibitor of protein tyrosine kinase, genistein, suppresses the effect of H2S, suggesting that tyrosine kinase may be involved in the enhancement of reducing activity by H2S. The H2S-specific enhancement of the reducing activity in neurons may lead to a neurotrophic role in the brain.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Astrocytes / drug effects
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Brain / cytology
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Brain / physiology*
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COS Cells
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Cell Line, Tumor
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Cells, Cultured
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Chlorocebus aethiops
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Dose-Response Relationship, Drug
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Embryo, Mammalian
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Genes, Reporter
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Genistein / pharmacology
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Hydrogen Sulfide / antagonists & inhibitors
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Hydrogen Sulfide / pharmacology*
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Luciferases / metabolism
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Mice
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NIH 3T3 Cells
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Neuroblastoma / pathology
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Neurons / cytology
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Neurons / drug effects*
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Oxidation-Reduction / drug effects
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Protein Kinase Inhibitors / pharmacology
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Rats
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Rats, Sprague-Dawley
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Tetrazolium Salts / metabolism
Substances
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Protein Kinase Inhibitors
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Tetrazolium Salts
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Genistein
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Luciferases
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Hydrogen Sulfide