Holloway 2018 Cell Rep

From Bioblast
Jump to: navigation, search
Publications in the MiPMap
Holloway GP, Holwerda AM, Miotto PM, Dirks ML, Verdijk LB, van Loon LJC (2018) Age-associated impairments in mitochondrial ADP sensitivity contribute to redox stress in senescent human skeletal muscle. Cell Rep 22:2837–48.

» Open Access

Holloway GP, Holwerda AM, Miotto PM, Dirks ML, Verdijk LB, van Loon LJC (2018) Cell Rep

Abstract: It remains unknown if mitochondrial bioenergetics are altered with aging in humans. We established an in vitro method to simultaneously determine mitochondrial respiration and H2O2 emission in skeletal muscle tissue across a range of biologically relevant ADP concentrations. Using this approach, we provide evidence that, although the capacity for mitochondrial H2O2 emission is not increased with aging, mitochondrial ADP sensitivity is impaired. This resulted in an increase in mitochondrial H2O2 and the fraction of electron leak to H2O2, in the presence of virtually all ADP concentrations examined. Moreover, although prolonged resistance training in older individuals increased muscle mass, strength, and maximal mitochondrial respiration, exercise training did not alter H2O2 emission rates in the presence of ADP, the fraction of electron leak to H2O2, or the redox state of the muscle. These data establish that a reduction in mitochondrial ADP sensitivity increases mitochondrial H2O2 emission and contributes to age-associated redox stress.

Keywords: Amplex Red in muscle fibers, Buffer Z, Blebbistatin Bioblast editor: Kandolf G O2k-Network Lab: CA Guelph Holloway GP


Labels: MiParea: Respiration  Pathology: Aging;senescence  Stress:Oxidative stress;RONS  Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Regulation: ADP  Coupling state: LEAK, OXPHOS, ET  Pathway: N, S, NS  HRR: Oxygraph-2k, O2k-Fluorometer 

2018-03, Amplex UltraRed