Difference between revisions of "Huetter 2007 Aging Cell"
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|preparations=Permeabilized tissue | |preparations=Permeabilized tissue | ||
|kinetics=ADP; Pi | |kinetics=ADP; Pi | ||
|topics=Ion | |topics=Ion homeostasis | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} | ||
==Discussion== | ==Discussion== | ||
* [[Gnaiger 2009 Int J Biochem Cell Biol]] | * [[Gnaiger 2009 Int J Biochem Cell Biol]] | ||
Revision as of 16:15, 6 August 2013
| Hütter E, Skovbro M, Lener B, Prats C, Rabol R, Dela F, Jansen-Dürr P (2007) Oxidative stress and mitochondrial impairment can be separated from lipofuscin accumulation in aged human skeletal muscle. Aging Cell 6: 245-256. |
Huetter E, Skovbro M, Lener B, Prats C, Rabol R, Dela F, Jansen-Duerr P (2007) Aging Cell
Abstract: According to the free radical theory of aging, reactive oxygen species (ROS) act as a driving force of the aging process, and it is generally believed that mitochondrial dysfunction is a major source of increased oxidative stress in tissues with high content of mitochondria, such as muscle or brain. However, recent experiments in mouse models of premature aging have questioned the role of mitochondrial ROS production in premature aging. To address the role of mitochondrial impairment and ROS production for aging in human muscles, we have analyzed mitochondrial properties in muscle fibres isolated from the vastus lateralis of young and elderly donors. Mitochondrial respiratory functions were addressed by high-resolution respirometry, and ROS production was analyzed by in situ staining with the redox-sensitive dye dihydroethidium. We found that aged human skeletal muscles contain fully functional mitochondria and that the level of ROS production is higher in young compared to aged muscle. Accordingly, we could not find any increase in oxidative modification of proteins in muscle from elderly donors. However, the accumulation of lipofuscin was identified as a robust marker of human muscle aging. The data support a model, where ROS-induced molecular damage is continuously removed, preventing the accumulation of dysfunctional mitochondria despite ongoing ROS production.
• O2k-Network Lab: AT_Innsbruck_Jansen-Duerr P, DK_Copenhagen_Dela F
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., Mitochondrial Disease; Degenerative Disease and Defect"Mitochondrial Disease; Degenerative Disease and Defect" 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: Human Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue
Regulation: Ion homeostasis"Ion homeostasis" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k
