Zelenka 2015 Oxid Med Cell Longev: Difference between revisions
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{{Publication | {{Publication | ||
|title=Zelenka J, DvoΕΓ‘k A, AlΓ‘n L (2015) L-lactate protects skin fibroblasts against aging-associated mitochondrial dysfunction via mitohormesis. Oxid Med Cell Longev 2015:351698. Β | |title=Zelenka J, DvoΕΓ‘k A, AlΓ‘n L (2015) L-lactate protects skin fibroblasts against aging-associated mitochondrial dysfunction via mitohormesis. Oxid Med Cell Longev 2015:351698. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/26171114 PMID: 26171114 Open Access] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/26171114 PMID: 26171114 Open Access] | ||
|authors=Zelenka J, Dvorak A, Alan L | |authors=Zelenka J, Dvorak A, Alan L | ||
|year=2015 | |year=2015 | ||
|journal=Oxid Med Cell Longev | |journal=Oxid Med Cell Longev | ||
|abstract=A moderate elevation of reactive oxygen species (ROS) production and a mild inhibition of mitochondrial respiratory chain have been associated with a health promotion and a lifespan extension in several animal models of aging. Here, we tested whether this phenomenon called mitohormesis could be mediated by L-lactate. The treatment with 5βmM L-lactate significantly increased H<sub>2</sub>O<sub>2</sub> production and slightly inhibited the respiration in cultured skin fibroblasts and in isolated mitochondria. The L-lactate exposure was associated with oxidation of intracellular glutathione, phosphorylation of 5'AMP-activated protein kinase (AMPK), and induction of peroxisome proliferator-activated receptor gamma coactivator 1Ξ± (PGC1Ξ±) transcription. A replicative aging of fibroblasts (L0) with a constant (LC), or intermittent 5βmM L-lactate (LI) in media showed that the high-passage LI fibroblasts have higher respiration, lower H<sub>2</sub>O<sub>2</sub> release, and lower secretion of L-lactate compared to L0 and LC. This protection against mitochondrial dysfunction in LI cells was associated with lower activity of mechanistic target of rapamycin complex 1 (mTORC1), less signs of cellular senescence, and increased autophagy compared to L0 and LC. In conclusion, we demonstrated that intermittent but not constant exposure to L-lactate triggers mitohormesis, prevents aging-associated mitochondrial dysfunction, and improves other markers of aging. Β | |abstract=A moderate elevation of reactive oxygen species (ROS) production and a mild inhibition of mitochondrial respiratory chain have been associated with a health promotion and a lifespan extension in several animal models of aging. Here, we tested whether this phenomenon called mitohormesis could be mediated by L-lactate. The treatment with 5βmM L-lactate significantly increased H<sub>2</sub>O<sub>2</sub> production and slightly inhibited the respiration in cultured skin fibroblasts and in isolated mitochondria. The L-lactate exposure was associated with oxidation of intracellular glutathione, phosphorylation of 5'AMP-activated protein kinase (AMPK), and induction of peroxisome proliferator-activated receptor gamma coactivator 1Ξ± (PGC1Ξ±) transcription. A replicative aging of fibroblasts (L0) with a constant (LC), or intermittent 5βmM L-lactate (LI) in media showed that the high-passage LI fibroblasts have higher respiration, lower H<sub>2</sub>O<sub>2</sub> release, and lower secretion of L-lactate compared to L0 and LC. This protection against mitochondrial dysfunction in LI cells was associated with lower activity of mechanistic target of rapamycin complex 1 (mTORC1), less signs of cellular senescence, and increased autophagy compared to L0 and LC. In conclusion, we demonstrated that intermittent but not constant exposure to L-lactate triggers mitohormesis, prevents aging-associated mitochondrial dysfunction, and improves other markers of aging. | ||
|mipnetlab=CZ Prague Jezek P | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, mtDNA;mt-genetics | |area=Respiration, mtDNA;mt-genetics | ||
|diseases=Aging;senescence | |||
|injuries=Oxidative stress;RONS | |||
|organism=Rat | |organism=Rat | ||
|tissues=Liver, Endothelial;epithelial;mesothelial cell | |tissues=Liver, Endothelial;epithelial;mesothelial cell, Fibroblast | ||
|preparations=Intact cells, Isolated mitochondria | |||
|preparations=Isolated mitochondria | |couplingstates=LEAK, ROUTINE, ET | ||
|pathways=N, S | |||
|couplingstates=LEAK, | |||
| | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Latest revision as of 16:37, 13 November 2017
| Zelenka J, DvoΕΓ‘k A, AlΓ‘n L (2015) L-lactate protects skin fibroblasts against aging-associated mitochondrial dysfunction via mitohormesis. Oxid Med Cell Longev 2015:351698. |
Zelenka J, Dvorak A, Alan L (2015) Oxid Med Cell Longev
Abstract: A moderate elevation of reactive oxygen species (ROS) production and a mild inhibition of mitochondrial respiratory chain have been associated with a health promotion and a lifespan extension in several animal models of aging. Here, we tested whether this phenomenon called mitohormesis could be mediated by L-lactate. The treatment with 5βmM L-lactate significantly increased H2O2 production and slightly inhibited the respiration in cultured skin fibroblasts and in isolated mitochondria. The L-lactate exposure was associated with oxidation of intracellular glutathione, phosphorylation of 5'AMP-activated protein kinase (AMPK), and induction of peroxisome proliferator-activated receptor gamma coactivator 1Ξ± (PGC1Ξ±) transcription. A replicative aging of fibroblasts (L0) with a constant (LC), or intermittent 5βmM L-lactate (LI) in media showed that the high-passage LI fibroblasts have higher respiration, lower H2O2 release, and lower secretion of L-lactate compared to L0 and LC. This protection against mitochondrial dysfunction in LI cells was associated with lower activity of mechanistic target of rapamycin complex 1 (mTORC1), less signs of cellular senescence, and increased autophagy compared to L0 and LC. In conclusion, we demonstrated that intermittent but not constant exposure to L-lactate triggers mitohormesis, prevents aging-associated mitochondrial dysfunction, and improves other markers of aging.
β’ O2k-Network Lab: CZ Prague Jezek P
Labels: MiParea: Respiration, mtDNA;mt-genetics
Pathology: Aging;senescence
Stress:Oxidative stress;RONS
Organism: Rat
Tissue;cell: Liver, Endothelial;epithelial;mesothelial cell, Fibroblast
Preparation: Intact cells, Isolated mitochondria
Coupling state: LEAK, ROUTINE, ET
Pathway: N, S
HRR: Oxygraph-2k
