Title |
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Pyrroloquinoline quinone prevents oxidative stress-induced neuronal death probably through changes in oxidative status of DJ-1.
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Creator |
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Accessrights |
open access |
Subject |
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Other
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DJ-1
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Other
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pyrroloquinoline quinone
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Other
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oxidative stress
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Other
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neurotoxity
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MeSH
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Animals
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MeSH
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Antioxidants/pharmacology
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MeSH
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Ascorbic Acid/pharmacology
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MeSH
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Blotting, Western
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MeSH
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Cell Death/drug effects
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MeSH
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Cell Survival/drug effects
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MeSH
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Dose-Response Relationship, Drug
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MeSH
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Female
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MeSH
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Hydrogen Peroxide/antagonists & inhibitors
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MeSH
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Hydrogen Peroxide/toxicity
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MeSH
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Microtubule-Associated Proteins/drug effects
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MeSH
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Microtubule-Associated Proteins/genetics
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MeSH
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Microtubule-Associated Proteins/metabolism
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MeSH
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Neurons/drug effects
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MeSH
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Oxidants/antagonists & inhibitors
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MeSH
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Oxidants/toxicity
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MeSH
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Oxidation-Reduction
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MeSH
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Oxidative Stress/drug effects
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MeSH
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Oxidopamine/antagonists & inhibitors
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MeSH
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Oxidopamine/toxicity
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MeSH
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Pregnancy
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MeSH
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Protein Binding
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MeSH
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Pyrroles/pharmacology
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MeSH
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Quinolines/pharmacology
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MeSH
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Rats
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MeSH
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Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
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MeSH
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Tetrazolium Salts
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MeSH
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Thiazoles
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MeSH
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Tumor Cells, Cultured
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MeSH
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Vitamin E/pharmacology
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NDC
499
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Description |
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Abstract
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Pyrroloquinoline quinone (PQQ) has been shown to play a role as an anti-oxidant in neuronal cells and prevent neuronal cell death in a rodent stroke model. DJ-1, a causative gene product for a familial form of Parkinson's disease, plays a role in anti-oxidative stress function by self-oxidation of DJ-1. In this study, the expression level and oxidation status of DJ-1 were examined in SHSY-5Y cells and primary cultured neurons treated with 6-hydroxydopamine (6-OHDA) or H(2)O(2) in the presence or absence of PQQ. The pI shift of DJ-1 to an acidic point, which was observed in SHSY-5Y cells treated with 6-OHDA, was inhibited by PQQ. TOF-MS analyses showed that while the level of a reduced form of DJ-1, one of the active forms of DJ-1, was decreased in SHSY-5Y cells treated with 6-OHDA or H(2)O(2), PQQ increased the level of the reduced form of DJ-1. These results suggest that PQQ prevents oxidative stress-induced changes in oxidative status of DJ-1. Therefore, the neuroprotective effects of PQQ on oxidative stress-induced neuronal death may be at least in part involved in increased level of an active form of DJ-1.
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Publisher |
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The Pharmaceutical Society of Japan
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Date |
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Language |
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Resource Type |
journal article |
Version Type |
VoR |
Identifier |
HDL
http://hdl.handle.net/2115/53726
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Relation |
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isIdenticalTo
DOI
https://doi.org/10.1248/bpb.31.1321
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PMID
18591768
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Journal |
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Biological & pharmaceutical bulletin
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Volume Number31
Issue Number7
Page Start1321
Page End1326
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File |
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Oaidate |
2023-07-26 |