Lifelong treatment with atenolol decreases membrane fatty acid unsaturation and oxidative stress in heart and skeletal muscle mitochondria and improves immunity and behavior, without changing mice longevity
dc.contributor.author | Gómez, Alexia | |
dc.contributor.author | Sánchez Román, Inés | |
dc.contributor.author | Gómez, Jose | |
dc.contributor.author | Cruces, Julia | |
dc.contributor.author | Mate Otaño, Ianire | |
dc.contributor.author | López Torres, Mónica | |
dc.contributor.author | Naudi, Alba | |
dc.contributor.author | Portero Otín, Manuel | |
dc.contributor.author | Pamplona, Reinald | |
dc.contributor.author | De la Fuente, Mónica | |
dc.contributor.author | Barja, Gustavo | |
dc.date.accessioned | 2024-02-09T06:39:36Z | |
dc.date.available | 2024-02-09T06:39:36Z | |
dc.date.issued | 2014 | |
dc.identifier.citation | Aging Cell 13 : 551-560 (2014) | |
dc.identifier.uri | http://hdl.handle.net/10810/65851 | |
dc.description.abstract | The membrane fatty acid unsaturation hypothesis of aging and longevity is experimentally tested for the first time in mammals. Lifelong treatment of mice with the β1-blocker atenolol increased the amount of the extracellular-signal-regulated kinase signaling protein and successfully decreased one of the two traits appropriately correlating with animal longevity, the membrane fatty acid unsaturation degree of cardiac and skeletal muscle mitochondria, changing their lipid profile toward that present in much more longer-lived mammals. This was mainly due to decreases in 22:6n-3 and increases in 18:1n-9 fatty acids. The atenolol treatment also lowered visceral adiposity (by 24%), decreased mitochondrial protein oxidative, glycoxidative, and lipoxidative damage in both organs, and lowered oxidative damage in heart mitochondrial DNA. Atenolol also improved various immune (chemotaxis and natural killer activities) and behavioral functions (equilibrium, motor coordination, and muscular vigor). It also totally or partially prevented the aging-related detrimental changes observed in mitochondrial membrane unsaturation, protein oxidative modifications, and immune and behavioral functions, without changing longevity. The controls reached 3.93 years of age, a substantially higher maximum longevity than the best previously described for this strain (3.0 years). Side effects of the drug could have masked a likely lowering of the endogenous aging rate induced by the decrease in membrane fatty acid unsaturation. We conclude that it is atenolol that failed to increase longevity, and likely not the decrease in membrane unsaturation induced by the drug. | |
dc.description.sponsorship | his investigation was supported by I + D grants from the Spanish Ministry of Science and Innovation (BFU2011-23888 to G.Barja); UCM Groups of Research (910379ENEROINN), BFU2011-30336, and RETICEF (RD 12/0043/0018) from ISCIII-FEDER of the European Union to M. De la Fuente; Spanish Ministry of Health (PI11/01532) to M.Portero Otin; and Spanish Ministry of Science and Innovation (BFU2009-11879) and the Generalitat of Catalonia (2009SGR735) to R. Pamplona. | |
dc.language.iso | eng | es_ES |
dc.publisher | Wiley | |
dc.relation | info:eu-repo/grantAgreement/MINECO/BFU2011-23888 | |
dc.relation | info:eu-repo/grantAgreement/MINECO/BFU2009-11879 | |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | |
dc.subject | aging | |
dc.subject | atenolol | |
dc.subject | fatty acid unsaturation | |
dc.subject | heart rate | |
dc.subject | longevity | |
dc.subject | oxidative stress | |
dc.title | Lifelong treatment with atenolol decreases membrane fatty acid unsaturation and oxidative stress in heart and skeletal muscle mitochondria and improves immunity and behavior, without changing mice longevity | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.rights.holder | © 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. | |
dc.relation.publisherversion | https://onlinelibrary.wiley.com/doi/10.1111/acel.12205 | |
dc.identifier.doi | 10.1111/acel.12205 | |
dc.departamentoes | Inmunología, microbiología y parasitología | |
dc.departamentoeu | Immunologia, mikrobiologia eta parasitologia | |
dc.identifier.eissn | 1474-9726 |
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Except where otherwise noted, this item's license is described as © 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.