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Molecular hydrogen suppresses free-radical-induced cell death by mitigating fatty acid peroxidation and mitochondrial dysfunction.

Authors
  • Iuchi, Katsuya1, 2
  • Nishimaki, Kiyomi1
  • Kamimura, Naomi1
  • Ohta, Shigeo1, 3
  • 1 Department of Biochemistry and Cell Biology, Graduate School of Medicine, Nippon Medical School, 1-396 Kosugi-machi, Nakahara-ku, Kawasaki-city, Kanagawa 211-8533, Japan. , (Japan)
  • 2 Department of Materials and Life Science, Faculty of Science and Technology, Seikei University, 3-3-1 Kichijojikitamachi, Musashino-shi, Tokyo, 180-8633, Japan. , (Japan)
  • 3 Department of Neurology Medicine, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan. , (Japan)
Type
Published Article
Journal
Canadian Journal of Physiology and Pharmacology
Publisher
Canadian Science Publishing
Publication Date
Oct 01, 2019
Volume
97
Issue
10
Pages
999–1005
Identifiers
DOI: 10.1139/cjpp-2018-0741
PMID: 31295412
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Molecular hydrogen (H2) was believed to be an inert and nonfunctional molecule in mammalian cells; however, we overturned the concept by reporting the therapeutic effects of H2 against oxidative stress. Subsequently, extensive studies revealed multiple functions of H2 by exhibiting the efficacies of H2 in various animal models and clinical studies. Here, we investigated the effect of H2 on free-radical-induced cytotoxicity using tert-butyl hydroperoxide in a human acute monocytic leukemia cell line, THP-1. Cell membrane permeability was determined using lactate dehydrogenase release assay and Hoechst 33342 and propidium iodide staining. Fatty acid peroxidation and mitochondrial viability were measured using 2 kinds of fluorescent dyes, Liperfluo and C11-BODIPY, and using the alamarBlue assay based on the reduction of resazurin to resorufin by mainly mitochondrial succinate dehydrogenase, respectively. Mitochondrial membrane potential was evaluated using tetramethylrhodamine methyl ester. As a result, H2 protected the cultured cells against the cytotoxic effects induced by tert-butyl hydroperoxide; H2 suppressed cellular fatty acid peroxidation and cell membrane permeability, mitigated the decline in mitochondrial oxidoreductase activity and mitochondrial membrane potential, and protected cells against cell death evaluated using propidium iodide staining. These results suggested that H2 suppresses free-radical-induced cell death through protection against fatty acid peroxidation and mitochondrial dysfunction.

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