Guachalla 2009 Aging (Albany NY)

Guachalla LM, Ju Z, Koziel R, Figura G, Song Z, Fusser M, Epe B,Jansen-Dürr P,Rudolph KL (2009) Sod2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice. Aging 1: 3.

» PMID: 20195488

Guachalla LM, Ju Z, Koziel R, Figura G, Song Z, Fusser M, Epe B, Jansen-Duerr P, Rudolph KL (2009) Aging

Abstract: Telomere shortening represents a causal factor of cellular senescence. At the same time, several lines of evidenceindicate a pivotal role of oxidative DNA damage for the aging process in vivo. A causal connection between the twoobservations was suggested by experiments showing accelerated telomere shorting under conditions of oxidative stress incultured cells, but has never been studied in vivo. We therefore have analysed whether an increase in mitochondrialderived oxidative stress in response to heterozygous deletion of superoxide dismutase (Sod2+/‐) would exacerbate agingphenotypes in telomere dysfunctional (mTerc‐/‐) mice. Heterozygous deletion of Sod2 resulted in reduced SOD2 proteinlevels and increased oxidative stress in aging telomere dysfunctional mice, but this did not lead to an increase in basallevels of oxidative nuclear DNA damage, an accumulation of nuclear DNA breaks, or an increased rate of telomereshortening in the mice. Moreover, heterozygous deletion of Sod2 did not accelerate the depletion of stem cells and theimpairment in organ maintenance in aging mTerc‐/‐ mice. In agreement with these observations, Sod2 haploinsufficiencydid not lead to a further reduction in lifespan of mTerc‐/‐ mice. Together, these results indicate that a decrease in SOD2‐dependent antioxidant defence does not exacerbate aging in the context of telomere dysfunction. • Keywords: Oxidative stress, Superoxide, Telomere shortening, Aging, DNA damage, SOD2, Free radicals, Stem cells

• O2k-Network Lab: AT_Innsbruck_Jansen Duerr P

Labels:

Stress: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., Genetic Defect; Knockdown; Overexpression"Genetic Defect; Knockdown; Overexpression" 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: Neurons; Brain"Neurons; Brain" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.  Preparation: Intact Cell; Cultured; Primary"Intact Cell; Cultured; Primary" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.  Enzyme: Uncoupling protein  Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" 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., Redox State"Redox State" 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