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| Research article summary (published 15 Sep 2009): |
Molecular hydrogen suppresses FcepsilonRI-mediated signal transduction and prevents degranulation of mast cells.
Full Abstract
Molecular hydrogen ameliorates oxidative stress-associated diseases in animal models. We found that oral intake of hydrogen-rich water abolishes an immediate-type allergic reaction in mice. Using rat RBL-2H3 mast cells, we demonstrated that hydrogen attenuates phosphorylation of the FcepsilonRI-associated Lyn and its downstream signal transduction, which subsequently inhibits the NADPH oxidase activity and reduces the generation of hydrogen peroxide. We also found that inhibition of NADPH oxidase attenuates phosphorylation of Lyn in mast cells, indicating the presence of a feed-forward loop that potentiates the allergic responses. Hydrogen accordingly inhibits all tested signaling molecule(s) in the loop. Hydrogen effects have been solely ascribed to exclusive removal of hydroxyl radical. In the immediate-type allergic reaction, hydrogen exerts its beneficial effect not by its radical scavenging activity but by modulating a specific signaling pathway. Effects of hydrogen in other diseases are possibly mediated by modulation of yet unidentified signaling pathways. Our studies also suggest that hydrogen is a gaseous signaling molecule like nitric oxide.
Author information
Author/s: Itoh, Tomohiro (T); Fujita, Yasunori (Y); Ito, Mikako (M); Masuda, Akio (A); Ohno, Kinji (K); Ichihara, Masatoshi (M); Kojima, Toshio (T); Nozawa, Yoshinori (Y); Ito, Masafumi (M);
Affiliation: Department of Longevity and Aging Research, Gifu International Institute of Biotechnology, 1-1 Naka-fudogaoka, Kakamigahara, Gifu, Japan.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun), published in United States. (Language: eng)
Reference: 2009-Nov; vol 389 (issue 4) : pp 651-6
Dates: Created 2009/10/14; Completed 2009/11/02;
PMID: 19766097, status: MEDLINE (last retrieval date: 11/2/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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