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Title
  • en Pyrroloquinoline quinone prevents oxidative stress-induced neuronal death probably through changes in oxidative status of DJ-1.
Creator
    • en Nunome, Kana
    • en Miyazaki, Shin
    • en Nakano, Masahiko
Accessrights open access
Subject
  • Other en DJ-1
  • Other en pyrroloquinoline quinone
  • Other en oxidative stress
  • Other en neurotoxity
  • MeSH en Animals
  • MeSH en Antioxidants/pharmacology
  • MeSH en Ascorbic Acid/pharmacology
  • MeSH en Blotting, Western
  • MeSH en Cell Death/drug effects
  • MeSH en Cell Survival/drug effects
  • MeSH en Dose-Response Relationship, Drug
  • MeSH en Female
  • MeSH en Hydrogen Peroxide/antagonists & inhibitors
  • MeSH en Hydrogen Peroxide/toxicity
  • MeSH en Microtubule-Associated Proteins/drug effects
  • MeSH en Microtubule-Associated Proteins/genetics
  • MeSH en Microtubule-Associated Proteins/metabolism
  • MeSH en Neurons/drug effects
  • MeSH en Oxidants/antagonists & inhibitors
  • MeSH en Oxidants/toxicity
  • MeSH en Oxidation-Reduction
  • MeSH en Oxidative Stress/drug effects
  • MeSH en Oxidopamine/antagonists & inhibitors
  • MeSH en Oxidopamine/toxicity
  • MeSH en Pregnancy
  • MeSH en Protein Binding
  • MeSH en Pyrroles/pharmacology
  • MeSH en Quinolines/pharmacology
  • MeSH en Rats
  • MeSH en Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
  • MeSH en Tetrazolium Salts
  • MeSH en Thiazoles
  • MeSH en Tumor Cells, Cultured
  • MeSH en Vitamin E/pharmacology
  • NDC 499
Description
  • Abstract en 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.
Publisher en The Pharmaceutical Society of Japan
Date
    Issued2008-07
Language
  • eng
Resource Type journal article
Version Type VoR
Identifier HDL http://hdl.handle.net/2115/53726
Relation
  • isIdenticalTo DOI https://doi.org/10.1248/bpb.31.1321
  • PMID 18591768
Journal
    • PISSN 0918-6158
      • en Biological & pharmaceutical bulletin
      • Volume Number31 Issue Number7 Page Start1321 Page End1326
File
Oaidate 2023-07-26