A model of metabolic changes in respiration-deficient human cells.
Cells lacking aerobic metabolism because of damaged mtDNA accumulate in many postmitotic tissues in the course aging. Although being only a small fraction of cells, they might play a major role in oxidative stress affecting the whole body. However, it remains unclear how such cells, which are under normal circumstances dependent on aerobic metabolism, are able to survive for decades in vivo. Here a new model is presented that proposes a coexistence of anaerobic glycolysis and a partly reversed TCA cycle. Succinate plays a key role in the changed metabolic pathways because it has to be exported by the cell. This hypothesis supports the view that some respiration-deficient cells are able to survive permanently within the body and contribute to human aging.
Bollmann
F Mathias
FM
Gymnasium Carolinum, Osnabrück, Germany. f.mathiasbollmann@web.de
D000375:Aging; D019069:Cell Respiration; D016922:Cellular Senescence; D004272:DNA, Mitochondrial / Q000378:metabolism*; D006019:Glycolysis; D006801:Humans; D008954:Models, Biological; D008962:Models, Theoretical; D018384:Oxidative Stress; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption; D010829:Physiological Phenomena; D019802:Succinic Acid / Q000378:metabolism; D014233:Tricarboxylic Acids / Q000737:chemistry
D004272:DNA, Mitochondrial; D014233:Tricarboxylic Acids; D019802:Succinic Acid; D010100:Oxygen