Gomez Rodriguez 2013 Abstract IOC75: Difference between revisions
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|organism=Mouse | |organism=Mouse | ||
|tissues=Liver | |tissues=Liver | ||
|preparations=Isolated | |preparations=Isolated mitochondria | ||
|enzymes=Complex I, Complex II; | |enzymes=Complex I, Complex II;succinate dehydrogenase, Complex III | ||
|injuries=RONS | |injuries=Oxidative stress;RONS | ||
|diseases=Aging; senescence | |diseases=Aging;senescence | ||
|topics=Redox state, Fatty | |topics=Redox state, Fatty acid | ||
|couplingstates=LEAK | |couplingstates=LEAK | ||
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Latest revision as of 10:36, 13 February 2015
Gomez Rodriguez A (2013) Γ-adrenergic receptor signaling interruption with two Ξ²-blockers (atenolol or nebivolol) can modify different oxidative stress related parameters linked to longevity in mouse liver. Mitochondr Physiol Network 18.03. |
Link: IOC75 Open Access
Gomez Rodriguez A, Sanchez-Roman I, Naudi A, Lopez-Torres M, Pamplona R, Barja G (2013)
Event: IOC75
A new mammalian longevity model based on Γ-adrenergic receptor signaling interruption at the level of adenylyl cyclase has reported decreased bone and heart aging and mean and maximum longevity increases in AC5 KO (adenylyl cyclase 5 Knocking out) mice [1]. In order to clarify if an oxidative stress decrease could be involved, we first decided to mimic this model in a pharmacological way. We have previously treated C57BL/6 mice with the Ξ²1-selective blocker atenolol in the drinking water, and this decreased the global degree of membrane fatty acid unsaturation as well as various markers of protein oxidation and lipoxidation [2]. In the present study, we have tested if that effect is extensible to other tissues, like liver, and other Ξ²1-selective blockers, like nebivolol. We have treated C57BL/6 mice with atenolol in drinking water and with nebivolol through intraperitoneal injection. Atenolol treatment decreased ROS production at the level of complex III, which correlates with a decrease in the amount of this complex. Besides, atenolol was able to decrease the level of MDAL, a specific marker of lipoxidation-dependent damage to proteins which is known to be lower in long-lived animals. On the other hand, nebivolol treatment decreased the level of oxidative damage in mitochondrial DNA (a characteristic trait of long-lived animals), and increased the ratio pERK/total ERK which indicates effective blockade of the Ξ²-adrenergic signaling pathway. These results show the specificity of Ξ²-blockers by their specific target tissues, like heart, and the lower effect in other systemic organs, like liver.
- Yan L, Vatner DE, O'Connor JP, Ivessa A, Ge H, Chen W, Hirotani S, Ishikawa Y, Sadoshima J, Vatner SF (2007) Type 5 adenylyl cyclase disruption increases longevity and protects against stress. Cell 130: 247β258
- Sanchez-Roman I, Gomez J, Naudi A, Ayala V, Portero-OtΓn M, Lopez-Torres M, Pamplona R, Barja G (2010) The beta-blocker atenolol lowers the longevity-related degree of fatty acid unsaturation, decreases protein oxidative damage, and increases extracellular signal-regulated kinase signaling in the heart of C57BL/6 mice. Rejuv Res 13: 683β693
β’ Keywords: Ξ²-Blockers
Labels: MiParea: Respiration Pathology: Aging;senescence Stress:Oxidative stress;RONS Organism: Mouse Tissue;cell: Liver Preparation: Isolated mitochondria Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III Regulation: Redox state, Fatty acid Coupling state: LEAK
Affiliations and author contributions
Supported by a BFU2011-2388 Grant to GB
A. Gomez1, I. Sanchez-Roman1, A. NaudΓ2, M. LΓ³pez-Torres1, R. Pamplona2, G. Barja1.
(1) Department of Animal Physiology II, Faculty of Biological Sciences, Complutense University, Madrid 28040, ES
(2) Department of Experimental Medicine, Faculty of Medicine, University of Lleida-IRB, Lleida 25008, ES