Hydrogen Indirectly Suppresses Increases in Hydrogen Peroxide in Cytoplasmic Hydroxyl Radical-Induced Cells and Suppresses Cellular Senescence.


Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
21 Jan 2019
Historique:
received: 15 12 2018
revised: 16 01 2019
accepted: 18 01 2019
entrez: 24 1 2019
pubmed: 24 1 2019
medline: 2 5 2019
Statut: epublish

Résumé

Bacteria inhabiting the human gut metabolize microbiota-accessible carbohydrates (MAC) contained in plant fibers and subsequently release metabolic products. Gut bacteria produce hydrogen (H₂), which scavenges the hydroxyl radical (•OH). Because H₂ diffuses within the cell, it is hypothesized that H₂ scavenges cytoplasmic •OH (cyto •OH) and suppresses cellular senescence. However, the mechanisms of cyto •OH-induced cellular senescence and the physiological role of gut bacteria-secreted H₂ have not been elucidated. Based on the pyocyanin-stimulated cyto •OH-induced cellular senescence model, the mechanism by which cyto •OH causes cellular senescence was investigated by adding a supersaturated concentration of H₂ into the cell culture medium. Cyto •OH-generated lipid peroxide caused glutathione (GSH) and heme shortage, increased hydrogen peroxide (H₂O₂), and induced cellular senescence via the phosphorylation of ataxia telangiectasia mutated kinase serine 1981 (p-ATM

Identifiants

pubmed: 30669692
pii: ijms20020456
doi: 10.3390/ijms20020456
pmc: PMC6359316
pii:
doi:

Substances chimiques

Cyclin-Dependent Kinase Inhibitor p16 0
Cyclin-Dependent Kinase Inhibitor p21 0
Eukaryotic Initiation Factor-2 0
Activating Transcription Factor 4 145891-90-3
Hydroxyl Radical 3352-57-6
Hydrogen 7YNJ3PO35Z
Hydrogen Peroxide BBX060AN9V
Glutathione GAN16C9B8O

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Japan Society for the Promotion of Science (JSPS) KAKENHI Grant-in-Aid for Scientific Research (C)
ID : 18K05537

Déclaration de conflit d'intérêts

The authors declare no conflict of interest.

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Auteurs

Takahiro Sakai (T)

Laboratory of Physiological Chemistry, Faculty of Pharmacy, Takasaki University of Health and Welfare, 60 Nakaorui-machi, Takasaki, Gunma 370-0033, Japan. sakai@takasaki-u.ac.jp.

Ryosuke Kurokawa (R)

MiZ Co., Ltd., 2-19-15 Ofuna, Kamakura, Kanagawa 247-0056, Japan. r_kurokawa@e-miz.co.jp.

Shin-Ichi Hirano (SI)

MiZ Co., Ltd., 2-19-15 Ofuna, Kamakura, Kanagawa 247-0056, Japan. s_hirano@e-miz.co.jp.

Jun Imai (J)

Laboratory of Physiological Chemistry, Faculty of Pharmacy, Takasaki University of Health and Welfare, 60 Nakaorui-machi, Takasaki, Gunma 370-0033, Japan. jimai@takasaki-u.ac.jp.

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Classifications MeSH