Publication | Closed Access
Regulation of mitochondrial respiration in senescence
136
Citations
25
References
1972
Year
Mitochondrial OxidationMitochondrial BiologyRedox BiologyOxidative StressMitochondrial BiogenesisLongevityMitochondrial MembraneMitochondrial StructureMetabolic SignalingHealth SciencesBiochemistryMitochondrial DynamicCytochrome C OxidationMetabolomicsCell BiologyEnergy MetabolismMitochondrial FunctionPhysiologyMitochondrial RespirationCellular SenescenceMetabolismMedicine
Abstract The ADP‐stimulated (State 3) respiration of myocardial mitochondria with glutamate‐malate, glutamate‐pyruvate, palmitylcarnitine and β‐hydroxybutyrate as substrates declined in rats after the age of 20 months. There was no significant decline in pyruvate‐malate, α‐oxoglutarate, palmityl‐CoA, succinate and ascorbate cytochrome c oxidation. Skeletal muscle mitochondria from senescent animals showed a similar decline in glutamate‐malate oxidation but not in palmityl‐CoA, palmitylcarnitine, succinate and ascorbate‐cytochrome c oxidation. The controlled oxidation with ADP‐limiting (State 4) and the ADP/O ratio were not affected. The results indicate an alteration in the subtle regulatory capacity for mitochondrial oxidation in senescent rats. It is suggested that the alteration may be in certain anion transport and associated functions across the mitochondrial membrane or dehydrogenase activity.
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