Difference between revisions of "Gomez Rodriguez 2013 Abstract IOC75"
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{{Abstract | {{Abstract | ||
|title=Gomez Rodriguez A (2013) | |title=Gomez Rodriguez A (2013)ß-adrenergic receptor signaling interruption with two β-blockers (atenolol or nebivolol) can modify different oxidative stress related parameters linked to longevity in mouse liver. | ||
|info=[http://www.oroboros.at/index.php?id=ioc75_schroecken IOC75 Open Access] | |info=[http://www.oroboros.at/index.php?id=ioc75_schroecken IOC75 Open Access] | ||
|authors=Gomez | |authors=A. Gomez, I. Sanchez-Roman1, A. Naudí2, M. López-Torres1, R. Pamplona2, G. Barja1. | ||
|year=2013 | |year=2013 | ||
|event=[[IOC75]] | |event=[[IOC75]] | ||
|abstract=A new mammalian longevity model based on ß-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 (Yan et al, 2007). 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 β1-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 (Sanchez-Roman et al, 2010). In the present study, we have tested if that effect is extensible to other tissues, like liver, and other β1-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 β-adrenergic signaling pathway. These results show the specificity of β-blockers by their specific target tissues, like heart, and the lower effect in other systemic organs, like liver. | |||
Supported by a BFU2011-2388 Grant to GB | |||
|keywords=β-blockers, Aging, Mitochondria, Liver | |||
|mipnetlab=ES_Madrid_Barja G | |||
}} | |||
{{Labeling | |||
|instruments=Spectrophotometry, Spectrofluorometry | |||
|injuries=RONS; Oxidative Stress, Aging; Senescence | |||
|organism=Mouse | |||
|tissues=Liver | |||
}} | }} | ||
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1 Department of Animal Physiology II, Faculty of Biological Sciences, Complutense University, Madrid 28040, Spain | |||
2 Department of Experimental Medicine, Faculty of Medicine, University of Lleida-IRBLleida, Lleida 25008, Spain | |||
Revision as of 12:05, 14 March 2013
Gomez Rodriguez A (2013)ß-adrenergic receptor signaling interruption with two β-blockers (atenolol or nebivolol) can modify different oxidative stress related parameters linked to longevity in mouse liver. |
Link: IOC75 Open Access
A. Gomez, I. Sanchez-Roman1, A. Naudí2, M. López-Torres1, R. Pamplona2, G. Barja1. (2013)
Event: IOC75
A new mammalian longevity model based on ß-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 (Yan et al, 2007). 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 β1-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 (Sanchez-Roman et al, 2010). In the present study, we have tested if that effect is extensible to other tissues, like liver, and other β1-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 β-adrenergic signaling pathway. These results show the specificity of β-blockers by their specific target tissues, like heart, and the lower effect in other systemic organs, like liver. Supported by a BFU2011-2388 Grant to GB
• Keywords: β-blockers, Aging, Mitochondria, Liver
• O2k-Network Lab: ES_Madrid_Barja G
Labels:
Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Aging; Senescence"Aging; Senescence" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Mouse Tissue;cell: Liver
HRR: Spectrophotometry"Spectrophotometry" is not in the list (Oxygraph-2k, TIP2k, O2k-Fluorometer, pH, NO, TPP, Ca, O2k-Spectrophotometer, O2k-Manual, O2k-Protocol, ...) of allowed values for the "Instrument and method" property., Spectrofluorometry"Spectrofluorometry" is not in the list (Oxygraph-2k, TIP2k, O2k-Fluorometer, pH, NO, TPP, Ca, O2k-Spectrophotometer, O2k-Manual, O2k-Protocol, ...) of allowed values for the "Instrument and method" property.
Affiliations and author contributions
1 Department of Animal Physiology II, Faculty of Biological Sciences, Complutense University, Madrid 28040, Spain 2 Department of Experimental Medicine, Faculty of Medicine, University of Lleida-IRBLleida, Lleida 25008, Spain